Cancer seriously threatens the lives and health of people worldwide, and exosomes seem to play an important role in managing cancer effectively, which has attracted extensive attention from researchers in recent years. This study aimed to scientifically visualize exosomes research in cancer (ERC) through bibliometric analysis, reviewing the past, summarizing the present, and predicting the future, with a view to providing valuable insights for scholars and policy makers. Researches search and data collection from Web of Science Core Collection and clinical trial.gov. Calculations and visualizations were performed using Microsoft Excel, VOSviewer, Bibliometrix R-package, and CiteSpace. As of December 1, 2024, and March 8, 2025, we identified 8,001 ERC-related publications and 107 ERC-related clinical trials, with an increasing trend in annual publications. Our findings supported that China, Nanjing Medical University, and International Journal of Molecular Sciences were the most productive countries, institutions, and journals, respectively. Whiteside, Theresa L. had the most publications, while Théry, C was the most co-cited scholar. In addition, Cancer Research was the most co-cited journal. Spatial and temporal distribution of clinical trials was the same as for publications. High-frequency keywords were "extracellular vesicle," "microRNA" and "biomarker." Additional, "surface functionalization," "plant," "machine learning," "nanomaterials," "promotes metastasis," "engineered exosomes," and "macrophage-derived exosomes" were promising research topics. Our study comprehensively and visually summarized the structure, hotspots, and evolutionary trends of ERC. It would inspire subsequent studies from a macroscopic perspective and provide a basis for rational allocation of resources and identification of collaborations among researchers.

Exosomes derived from cancer-associated fibroblasts (CAFs) can affect tumor microenvironment (TME) of thyroid cancer (TC). The cAMP response element binding protein 1 (CREB1) acts as a transcription factor to participate in cancer development. Currently, we aimed to explore the molecular mechanism of exosome-associated CREB1 and C-C motif chemokine ligand 20 (CCL20) in TC.

The mRNA and protein levels were examined via RT-qPCR and western blot. Gene interaction was analyzed using ChIP and dual-luciferase reporter assays. Cell migration, invasion and proliferation were assessed by wound healing, transwell and EdU assays. Exosomes were characterized by morphology observation and western blot. The proliferation and apoptosis of CD8+ T cells were detected by immunofluorescence and flow cytometry. In vivo assays were performed by establishing xenograft models.

CREB1 was highly expressed in TC. CREB1 positively interacted with CCL20 in TC. CREB1 facilitated TC cell migration, invasion and proliferation via targeting CCL20. CCL20 expression was reduced by transferring CAFs-secreted exosomes sheltering CREB1 downregulation. Exosomal CREB1 knockdown receded cell progression and enhanced CD8+ T function by mediating CCL20. CAFs-associated exosomal CREB1 downregulation inhibited tumorigenesis through affecting CCL20.

CAFs-derived exosomes accelerated the malignant behaviors and immune evasion in TC by carrying CREB1 to up-regulate CCL20.

PD-L1+ exosomes act as a useful biomarker in early cancer diagnosis, therapeutic monitoring, prognostic assessment, and immunotherapy for non-invasive liquid biopsy. There exists urgent clinical need for developing rapid, portable, and cost-effective immediate-response assays for PD-L1+ exosomes. Here, we proposed a smartphone-assisted colorimetric sensor using the triple-helix molecular switch (THMS) combined with Y-shaped catalytic hairpin assembly (Y-CHA) reaction. Namely, this strategy initiates the Y-CHA cycle and forms Y-DNA G-quadruplex/Hemin DNAzyme with K+ and Hemin after specific recognition of PD-L1+ exosomes by THMS. Then, PD-L1+ exosomes could be quantified via the oxidation of 3,3',5,5'-tetramethylbenzidine (TMB)-mediated color change. The method demonstrates excellent specificity and sensitivity, with a limit of detection (LOD) of 5.45 × 103 particles/mL and an LOD of 8.56 × 103 particles/mL using smartphone analysis. With this strategy, we found that PD-L1+ exosome levels were significantly elevated in the peripheral blood of patients with colorectal cancer liver metastases (CRLM), indicating great potential for identifying CRLM patients. Additionally, this colorimetric sensor can be used to quantify PD-L1+ exosomes across wide range of cancers, which possess a great prospect in the point-of-care testing filed for cancer companion diagnosis.

Bacterial pathogens can cause severe infections leading to mortality and morbidity. The current method of treatment for bacteria is the use of multiple antibiotics. Due to the overuse of antibiotics, many bacteria have become antibiotic-resistant. An alternative and effective treatment for bacterial infection is needed, and photothermal therapy (PTT) has emerged as a new solution for treating bacterial infection. Similarly, one of the main challenges in cancer treatment is the overuse of drugs that have multiple side effects. In recent years, there have been significantly more research activities in alternative therapy for pathogenic bacteria and cancer cells. Recently, PTT has also been used to treat various medical conditions like cancer, bacterial infections, or bacterial biofilm. Different kinds of nanomaterials like gold nanoparticles (AuNPs), Graphene Oxide (GO), Carbon nanotubes (CNTs), etc. have been explored for this purpose. In this particular review, we will elaborate on different kinds of nanomaterials (metallic, non-metallic, polymeric) widely used for PTT applications for bacteria and cancer cells. These kinds of nanoparticles have strong absorption in the NIR region and can convert light energy into heat energy, leading to hyperthermia. Further different types of PTT will be elaborated on, along with challenges and future applications. The current review will pave a new way for the therapeutic potential of different nanomaterials for bacterial infection and cancer treatment.

Recent studies have revealed a great diversity and complexity in extracellular vesicles and particles (EVPs). The developments in techniques and the growing awareness of the particle heterogeneity have spurred active research on new particle subsets. Latest discoveries highlighted unique features and roles of non-vesicular extracellular nanoparticles (NVEPs) as promising biomarkers and targets for diseases. These nanoparticles are distinct from extracellular vesicles (EVs) in terms of their smaller particle sizes and lack of a bilayer membrane structure and they are enriched with diverse bioactive molecules particularly proteins and RNAs, which are widely reported to be delivered and packaged in exosomes. This review is focused on the two recently identified membraneless NVEPs, exomeres and supermeres, to provide an overview of their biogenesis and contents, particularly those bioactive substances linked to their bio-properties. This review also explains the concepts and characteristics of these nanoparticles, to compare them with other EVPs, especially EVs, as well as to discuss their isolation and identification methods, research interests, potential clinical applications and open questions.

Exosomes are nanoscale extracellular vesicles (EVs) secreted by most eukaryotic cells and can be found in nearly all human body fluids. Increasing evidence has revealed their pivotal roles in intercellular communication, and their active participation in myriad physiological and pathological activities. Exosomes' functions rely on their contents that are closely correlated with the biological characteristics of parental cells, which may provide a rich resource of molecular information for accurate and detailed diagnosis of a diverse array of diseases, such as differential diagnosis of Alzheimer's disease, early detection and subtyping of various tumors. As a category of sensitive detection devices, biosensors can fully reveal the molecular information and convert them into actionable clinical information. In this review, recent advances in biosensor-based methods for the detection of exosomes are summarized. We have described the fabrication of various biosensors based on the analysis of exosomal proteins, RNAs or glycans for accurate diagnosis, with respect to their elaborate recognition designs, signal amplification strategies, sensing properties, as well as their application potential. The challenges along with corresponding technologies in the future development and clinical translation of these biosensors are also discussed.

Exosomes encompass a great deal of valuable biological information and play a critical role in tumor development. However, the mechanism of exosomal lncRNAs remains poorly elucidated in bladder cancer (BCa). In this study, we identified exosomal lnc-TAF12-2:1 as a novel biomarker in BCa diagnosis and aimed to investigate the underlying biological function. Dual luciferase reporter assay, RNA immunoprecipitation (RIP), RNA pulldown assays, and xenograft mouse model were used to verify the competitive endogenous RNA mechanism of lnc-TAF12-2:1. We found exosomal lnc-TAF12-2:1 up-regulated in urinary exosomes, tumor tissues of patients, and BCa cells. Down-regulation of lnc-TAF12-2:1 impaired BCa cell proliferation and migration, and promoted cell cycle arrest at the G0/G1 phase and cell apoptosis. The opposite effects were also observed when lnc-TAF12-2:1 was overexpressed. lnc-TAF12-2:1 was transferred by intercellular exosomes to modulate malignant biological behavior. Mechanistically, lnc-TAF12-2:1 packaged in the exosomes relieved the miRNA-mediated silence effect on ASB12 via serving as a sponger of miR-7847-3p to accelerate progression in BCa. ASB12 was also first proved as an oncogene to promote cell proliferation and migration and depress cell cycle arrest and cell apoptosis in our data. In conclusion, exosomal lnc-TAF12-2:1, located in the cytoplasm of BCa, might act as a competitive endogenous RNA to competitively bind to miR-7847-3p, and then be involved in miR-7847-3p/ASB12 regulatory axis to promote tumorigenesis, which provided a deeper insight into the molecular mechanism of BCa.

Pancreatic cancer is one of the most malignant tumors with a grim prognosis. Patients develop chemoresistance that drastically decreases their survival. The chemoresistance is mainly attributed to deficient vascularization of the tumor, intratumoral heterogeneity and pathophysiological barrier due to the highly desmoplastic tumor microenvironment. The interactions of cells that constitute the tumor microenvironment change its architecture into a cancer-permissive environment and stimulate cancer development, metastasis and treatment response. The cell-cell communication in the tumor microenvironment is often mediated by exosomes that harbour a diverse repertoire of molecular cargo, such as proteins, lipids, and nucleic acid, including messenger RNAs, non-coding RNAs and DNA. Therefore, exosomes can serve as potential targets as biomarkers and improve the clinical management of pancreatic cancer to overcome chemoresistance. This review critically elucidates the role of exosomes in cell-cell communication within the tumor microenvironment and how these interactions can orchestrate chemoresistance.

Neuropilin-1 (NRP1) is a transmembrane glycoprotein that functions as a co-receptor with various cellular functions. Our previous studies identified the NRP1 exon 4-skipping (NRP1-ΔE4) splice variant as an aggressive metastasis driver by activating endosomal signals. Here, we demonstrate the critical role of glycosaminoglycan (GAG) modification in regulating NRP1-ΔE4's cellular trafficking and oncogenic activity. NRP1-ΔE4 undergoes constitutive internalization into endosomes and subsequent exosomal release from colorectal cancer (CRC) cells. Exosomal NRP1-ΔE4 enhances the migration and invasion of both donor and recipient CRC cells. Genetic or pharmacological inhibition of exosome secretion, or immunodepletion of exosomal NRP1-ΔE4, markedly reduces its metastatic potential. Notably, GAG modification at the O-glycosylation site Ser612 is essential for NRP1-ΔE4's endosomal trafficking and exosomal release. This modification also promotes the formation of a trimeric complex with Met and β1-integrin, leading to their co-internalization and accumulation in endosomes, which activates FAK signaling and drives CRC metastasis. These findings reveal GAG modification as a key regulatory process that governs the endosomal-exosomal trafficking of NRP1-ΔE4 to facilitate CRC cell dissemination.

Tumor-derived extracellular vesicles (tEVs), which are essential mediators for cell-to-cell communication during tumorigenesis and tumor development, have demonstrated significant diagnostic potential in cancer liquid biopsy, particularly through biomarkers like membrane proteins and inner microRNAs. However, traditional detection methods such as ELISA and qRT-PCR encounter challenges with low sensitivity and specificity, complex procedures, and high costs. Although emerging biosensors have been developed, these methods are limited to detecting a single type of tEV biomarker, which may result in misdiagnoses due to false-positive or false-negative signals. Herein, we introduce a specific and serum-stable membrane-fusion approach (SSMFA) capable of simultaneously detecting tEV proteins and microRNAs via dual-color fluorescence analysis. In this strategy, the established epithelial cell adhesion molecule (EpCAM) aptamer-modified serum-stable membrane-fusion liposome (AptSMFL) is labeled with fluorescence resonance energy transfer (FRET) dye pairs, which can specifically recognize EpCAM-overexpressed tEVs and induce serum-stable membrane fusion, allowing the quantification of EpCAM protein levels through red fluorescence changes resulting from FRET alterations. Meanwhile, SSMFA facilitates efficient transfection of the CRISPR/Cas13a probe into tEVs to analyze the levels of microRNA-21 (miR-21) in EpCAM-positive tEVs via green fluorescence detection. When tested on serum samples from hepatocellular carcinoma models, the SSMFA exhibited minimal sample volume requirement and rapid assay time (2 h) to effectively achieve accurate quantification of both tEV EpCAM protein and miR-21 levels. Additionally, this dual-biomarker detection method showed a strong correlation with tumor burden and significantly improved cancer diagnostic accuracy (AUC = 0.98), underscoring the potential of SSMFA as a promising tEV-based liquid biopsy assay for cancer diagnosis.

Breast cancer (BC) has become the primary cancer that threatens women's health and life expectancy. Early diagnosis is crucial for effective treatment and favourable prognosis. As a non-invasive and valuable liquid biopsy method, exosomes are promising for the diagnosis and prognosis of BC. The aim of this meta-analysis is to evaluate the diagnostic and prognostic value of exosome biomarkers in BC.

A systematic search of relevant English literature was conducted in PubMed, Web of Science, and Cochrane library until August 2024 (diagnosis) and October 2024 (prognosis). QUADAS-2 and QUAPAS were used to assess the quality of the literature. Summary statistics and analyses of relevant effect sizes were conducted using STATA software. Subgroup analysis and sensitivity analysis were performed to identify potential sources of heterogeneity.

For diagnosis, a total of 31 articles with 3,778 patients and 2,722 controls were included, the pooled sensitivity (SEN), specificity (SPE), and area under the receiver operating characteristic curve (AUC) of overall exosome biomarkers were 0.89 (95 %CI: 0.86-0.91), 0.87 (95 %CI: 0.85-0.90), and 0.94 (95 %CI: 0.92-0.96), respectively, indicating a high diagnostic value of exosomes in BC patients. Subgroup analysis suggested that miRNAs in exosomes exhibited better diagnostic value compared to proteins and non-miRNAs, the SEN, SPE, and AUC were 0.89 (95 %CI: 0.82-0.93), 0.86 (95 %CI: 0.80-0.90), and 0.92 (95 %CI: 0.90-0.94), respectively. Among all miRNAs, the pooled SEN, SPE, and AUC of miR-21 were 0.86 (95 %CI: 0.67-0.95), 0.90 (95 %CI: 0.78-0.96), and 0.95 (95 %CI: 0.92-0.96), respectively. The diagnostic efficiency was improved when biomarkers were combined as a panel (SEN 0.91 versus 0.87, SPE 0.89 versus 0.86, AUC 0.96 versus 0.91). In terms of prognosis, we retrieved 14 articles with 2,781 patients. The pooled HR of overall survival (OS) and progression-free survival (PFS) were 1.41 (95 %CI: 0.92-1.90) and 4.39 (95 %CI: 1.87-6.91), respectively, indicating exosome biomarkers like soluble HLA-G, miR-1246, miR-155, and PSMA were a predictor of poor PFS in BC patients. Subgroup analysis in OS group revealed a significant association between the overexpression of exosome proteins (soluble HLA-G, AnxA2, NGF, CXCL13) and worse OS in BC patients (HR = 2.91, 95 %CI: 1.36-4.47). Similarly, the overexpression of miR-1246 and miR-155 was associated with worse PFS in BC patients (HR = 4.13, 95 %CI: 1.24-7.03). Moreover, when biomarkers were combined as a panel, the prognostic efficiency significantly improved in OS (HR = 4.05, 95 %CI: 2.26-5.84) outcome.

The meta-analysis revealed that exosome miR-21 might serve as a promising diagnostic biomarker in BC. Dysregulated exosome proteins and miRNAs could predict poor OS and PFS outcomes, respectively.

Oviducts contain various nutrients that provide energy during oocyte development. This study aimed to improve the efficiency of in vitro reproduction using extracellular vesicles (EVs) produced by the oviduct epithelial cells of sika deer (Cervus nippon). Surprisingly, the uptake of deer oviduct epithelial cell extracellular vesicles (DOEC-EVs) by cumulus-oocyte complexes, which were encapsulated by dense cumulus cells (CCs), occurred only in CCs during maturation. Therefore, we hypothesized that DOEC-EVs are transported to oocytes through CCs to exert their effects. We first investigated the effects of DOEC-EVs on the expansion capacity of the cumulus-oocyte complexes, as well as cell cycle progression, proliferation, apoptosis, and lactate and pyruvate levels in CCs, and examined reactive oxygen species levels, mitochondrial function, and key gene expression. The results showed that DOEC-EVs regulated cell cycle progression, promoted proliferation, reduced apoptosis, and improved antioxidant capacity and glycolysis, and through the oocyte first polar body excretion rate, reactive oxygen levels, and mitochondrial membrane potential, it was shown that CC promoted in vitro oocyte maturation, improved the antioxidant capacity and mitochondrial function of oocytes, and promoted parthenogenetic embryo development. These results suggest that DOEC-EVs improve the efficiency of oocyte development in deer in vitro by acting on CCs, laying the foundation for further research on in vitro deer reproduction.

This study aimed to elucidate the underlying mechanisms regarding microRNA-708-5p (miR-708-5p) in lung adenocarcinoma (LUAD). Here, the co-culture system of LUAD cells and macrophages, as well as a xenograft mouse model, were established. High levels of miR-708-5p were observed in LUAD. Exosomal miR-708-5p facilitated M2-like phenotype polarization, whereas miR-708-5p inhibition blocked the polarization. Exosomal miR-708-5p was identified as a pivotal signaling molecule for macrophages to mediate tumor cell proliferation, invasion, migration and IFN-γ production in T cells. In addition, miR708-5p was observed to induce PD-L1 expression, and PD-L1 silencing inhibited macrophage-induced tumor cell growth behavior and regulated CD8 T cell activity. In xenograft models, miR-708-5p inhibition and PD-L1 silencing attenuated macrophage-induced tumor growth, induced IFN-γ secretion and CD8 expression, and modulated the PTEN/AKT/mTOR pathway. In LUAD patients, there was an upregulation of both miR-708-5p and PD-L1 expression, accompanied by the activation of PTEN/AKT/mTOR. In conclusion, this study demonstrated the induction of M2 macrophage polarization and PD-L1 expression by exosomal miR-708-5p. We observed that exosomal miR-708-5p mediated the PTEN/AKT/mTOR pathway, diminished CD8 T cell activity and accelerated LUAD progression. The inhibition of specific exosomal miRNA secretion and anti-PD-L1 in the LUAD microenvironment may represent a promising avenue for LUAD immunotherapy.

Colorectal cancer (CRC), a commonly diagnosed malignancy, is one of the most frequent causes of cancer-related deaths worldwide. To effectively lower the death rate from this disease, it is essential to create public health methods, including developing new biomarkers that facilitate screening, diagnosis, prognosis, and therapy response prediction. CRC-derived Exosomes are a type of extracellular vesicle that transport functional molecules like proteins, lipids, nucleic acids (DNA, mRNA, miRNA, lncRNA, and noncoding RNA), and other metabolites, which act as molecular cargos to facilitate transportation. Exosomes generated and secreted from cancer cells are key biomarkers for early, noninvasive cancer diagnosis, prognosis, and treatment response, with their biogenesis in CRC offering molecular insights. Their expression varies across time, tissues, and disease stages. Thus, the development of innovative and effective techniques for isolating and detecting exosomes holds great potential for tumor diagnosis, prognosis prediction, and developing techniques (MSC-derived exosome, DC-derived exosome, engineered exosome, etc.) and their contents to improve the specificity and efficacy of therapies for patients with CRC. This review explores the features and formation of CRC-derived exosomes, highlighting their diagnostic, prognostic, and therapeutic significance through a comprehensive analysis of exosome extraction, identification, purification, and documented biological roles in existing literature.

Exosomes, lipid bilayer nanovesicles secreted by nearly all cell types, play pivotal roles in intercellular communication by transferring proteins, nucleic acids, and lipids. This review comprehensively summarizes their multiple functions in inflammation and cancer. In inflammation, exosomes exhibit context-dependent pro- or anti-inflammatory effects: they promote acute responses by delivering cytokines and miRNAs to activate immune cells, yet suppress chronic inflammation via immunoregulatory molecules. Two representative inflammatory diseases, namely sepsis and inflammatory bowel disease, were highlighted to elucidate their roles in the acute and chronic inflammatory diseases. In cancer, exosomes orchestrate tumor microenvironment (TME) remodeling by facilitating angiogenesis, metastasis, and immune evasion through interactions with cancer-associated fibroblasts, tumor-associated macrophages, and extracellular matrix components. Furthermore, exosomes can facilitate the transition from inflammation to cancer by impacting pertinent signaling pathways via their transported oncogenic and inflammatory molecules. Tumor-derived exosomes also serve as non-invasive biomarkers correlating with disease progression. Clinically, exosomes demonstrate promise as therapeutic agents and drug carriers, evidenced by ongoing trials targeting inflammatory diseases and cancers. However, challenges in isolation standardization, scalable production, and understanding functional heterogeneity hinder clinical translation. Future research should prioritize elucidating cargo-specific mechanisms, optimizing engineering strategies, and advancing personalized exosome-based therapies. By bridging molecular insights with clinical applications, exosomes hold great potential in precision medicine for inflammation and oncology.

Extracellular Vesicles (EVs) from seminal plasma have achieved attention due to their potential physiopathological role in male reproductive systems. This study employed a comprehensive proteomic and transcriptomic approach to investigate the composition and molecular signatures of EVs isolated from human seminal plasma. EVs from Normozoospermic (NORMO), OligoAsthenoTeratozoospermic (OAT), and Azoospermic (AZO) subjects were isolated using a modified polymer precipitation-based protocol and characterized for size and morphology. Comprehensive proteomic analysis, using both gel-free and gel-based approaches, revealed distinct protein profiles in each group (p<0.01), highlighting potential molecules and pathways involved in sperm function and fertility. The data are available via ProteomeXchange with identifiers PXD051361 and PXD051390, respectively. Transcriptomic analysis confirmed the trend of a general downregulation of AZO and OAT compared to NORMO shedding light on regulatory mechanisms of sperm development. Bioinformatic tools were applied for functional omics analysis; the integration of proteomic and transcriptomic data provided a comprehensive understanding of the cargo content and regulatory networks present in EVs. This study contributes to elucidating the key role of EVs in the paracrine communication regulating spermatogenesis. A full understanding of these pathways not only suggests potential mechanisms regulating male fertility but also offers new insights into the development of diagnostic tools targeting male reproductive disorders.

The medial overall survival is low in patients with gastric cancer (GC) at advanced stage, in which drug resistance plays an important role. β-elemene has been established as the suppressed role on GC cell proliferation, however, the concrete mechanism of it remains unclear in cisplatin (DDP)-resistance GC. Cell counting kit-8 (CCK8) assay was used to measure the half maximal inhibitory concentration (IC50) values of DDP in DDP-resistance GC cell lines. Cell apoptotic rates and invasive ability were tested by flow cytometry and transwell assay. Western blot and reverse-transcription quantitative polymerase chain reaction (RT-qPCR) were utilized to detect the protein and mRNA levels of methyltransferase like-3 (METTL3) and ADP ribosylation factor 6 (ARF6). SRAMP websites and methylated RNA immunoprecipitation (MeRIP) assay were applied to predicted m6A sites and verified m6A levels of ARF6 respectively. RNA immunoprecipitation (RIP) was used to explore the interaction between these two molecules. Xenograft tumor models were constructed to demonstrate the effects of β-elemene in vivo. β-elemene improved drug sensitivity and curbed malignant cell activities of DDP-resistance GC cells in vitro. ARF6 was upregulated in DDP-resistance GC cells and tissues, and its overexpression could abrogate the effects on DDP-resistant GC cells mediated by β-elemene treatment. Intracellular and exosomal METLL3 expression were elevated in and from DDP-resistance GC cell lines. Exosomal METTL3 released from DDP-resistance GC cells could counteract the effects of β-elemene on DDP-resistance GC cells partly via regulating ARF6 expression in the m6A-dependent manner. β-elemene could suppress DDP-resistance tumor growth in vivo. In conclusion, β-elemene could repress tumor growth and drug resistance via exosomal METTL3-m6A-ARF6 axis.

Cancer remains a prominent worldwide health concern, presenting existing therapies with frequent difficulties, including major toxicity, limited effectiveness, and treatment resistance emergence. These issues highlight the necessity for novel and enhanced remedies. Exosomes, tiny extracellular vesicles that facilitate intercellular communication, have attracted interest for their potential medicinal applications. Carrying a variety of molecules, including microRNAs, small interfering RNAs, long non-coding RNAs, proteins, lipids, and DNA, these vesicles are positioned as promising cancer treatment options. Current studies have increasingly investigated the capacity of microRNAs as a strategic approach for combating malignancy. Mesenchymal stem cells (MSC) are recognized for their aptitude to augment blood vessel formation, safeguard against cellular death, and modulate immune responses. Consequently, researchers examine exosomes derived from MSCs as a safer, non-cellular choice over therapies employing MSCs, which risk undesirable differentiation. The focus is shifting towards employing miRNA-encapsulated exosomes sourced from MSCs to target and heal cancerous cells selectively. However, the exact functions of miRNAs within MSC-derived exosomes in the context of cancer are still not fully understood. Additional exploration is necessary to clarify the role of these miRNAs in malignancy progression and to pinpoint viable therapeutic targets. This review offers a comprehensive examination of exosomes derived from mesenchymal stem cells, focusing on the encapsulation of miRNAs, methods for enhancing cellular uptake and stability, and their potential applications in cancer treatment. It also addresses the difficulties linked to this methodology and considers future avenues, including insights from current clinical oncology research.

Cancer remains one of the most devastating diseases, severely affecting public health and contributing to economic instability. Researchers worldwide are dedicated to developing effective therapeutics to target cancer cells. One promising strategy involves inducing cellular senescence, a complex state in which cells exit the cell cycle. Senescence has profound effects on both physiological and pathological processes, influencing cellular systems through secreted factors that affect surrounding and distant cells. Among these factors are exosomes, small extracellular vesicles that play crucial roles in cellular communication, development, and defense, and can contribute to pathological conditions. Recently, there has been increasing interest in engineering exosomes as precise drug delivery vehicles, capable of targeting specific cells or intracellular components. Studies have emphasized the significant role of exosomes from senescent cells in cancer progression and therapy. Notably, chemotherapeutic agents can alter the tumor microenvironment, induce senescence, and trigger immune responses through exosome-mediated cargo transfer. This review explores the intricate relationship between cellular senescence, exosomes, and cancer, examining how different therapeutics can eliminate cancer cells or promote drug resistance. It also investigates the molecular mechanisms and signaling pathways driving these processes, highlighting current challenges and proposing future perspectives to uncover new therapeutic strategies for cancer treatment.

Cervical cancer (CC) remains a significant global health concern, particularly affecting women in low-income countries. Despite advancements in screening programs, CC continues to pose a substantial mortality risk, highlighting the need to explore diagnostic and treatment modalities. This review focuses on the role of deregulated microRNAs (miRNAs) in CC development, emphasizing their potential as biomarkers for early detection and prognosis in body fluids. miRNAs have emerged as critical regulators of key cellular processes, including proliferation, migration, invasion, and apoptosis, and their dysregulation is closely linked to CC progression. Upregulated miRNAs such as miR-146b-3p, miR-1908, and miR-21 promote CC progression by targeting tumor suppressor genes, while downregulated miRNAs like miR-23-3p and miR-4262 are associated with reduced tumor aggressiveness. miRNAs also hold significant promise as non-invasive prognostic biomarkers. Their expression levels correlate with clinical outcomes, including tumor stage, metastasis, and overall survival, making them valuable tools for risk stratification and personalized treatment strategies. Liquid biopsies, which detect circulating miRNAs in bodily fluids, offer a minimally invasive approach to monitor tumor dynamics and predict patient outcomes. Furthermore, exosomal miRNAs are emerging as promising diagnostic and prognostic tools for CC. Advanced diagnostic technologies and bioinformatics tools are anticipated to enhance the identification of evident miRNA biomarkers in the clinical settings. Standardized protocols for sample collection and analysis will improve the reproducibility of miRNA studies, while a deeper understanding of miRNA biology may unlock their potential as therapeutic targets. In conclusion, this review consolidates current research on deregulated miRNAs in CC, highlighting their diagnostic and prognostic significance. The findings underscore the potential of miRNAs to revolutionize CC management through innovative diagnostic and therapeutic strategies.

Autophagy and apoptosis are two essential mechanisms regulating cell fate. Although distinct, their signaling pathways are closely interconnected through various crosstalk mechanisms. Lipid rafts are described to act as both physical and functional platforms during the early stages of autophagic and apoptotic processes. Only recently has a role for lipid raft-associated molecules in regulating EV biogenesis and release begun to emerge. In particular, lipids of EV membranes are essential components in conferring stability to these vesicles in different extracellular environments and/or to facilitate binding or uptake into recipient cells. In this review we highlight these aspects, focusing on the role of lipid molecules during apoptosis and secretory autophagy pathways. We describe the molecular machinery that connects autophagy and apoptosis with vesicular trafficking and lipid metabolism during the release of EVs, and how their alterations contribute to the development of various diseases, including autoimmune disorders and cancer. Overall, these findings emphasize the complexity of autophagy/apoptosis crosstalk and its key role in cellular dynamics, supporting the role of lipid rafts as new therapeutic targets.

Inflammation is a complex, tightly regulated process involving biochemical and cellular reactions to harmful stimuli. Often termed "the internal fire", it is crucial for protecting the body and facilitating tissue healing. While inflammation is essential for survival, chronic inflammation can be detrimental, leading to tissue damage and reduced survival. The innate immune system triggers inflammation, closely linked to the development of heart diseases, with significant consequences for individuals. Inflammation in arterial walls or the body substantially contributes to atherosclerotic disease progression, affecting the cardiovascular system. Altered lipoproteins increase the risk of excessive blood clotting, a hallmark of atherosclerotic cardiovascular disease and its complications. Integrating inflammatory biomarkers with established risk assessment techniques can enhance our ability to identify at-risk individuals, assess their risk severity, and recommend appropriate CVD prevention strategies. Exosomes, a type of extracellular vesicle, are released by various cells and mediate cell communication locally and systemically. In the past decade, exosomes have been increasingly studied for their vital roles in health maintenance and disease processes. They can transport substances like non-coding RNAs, lipids, and proteins between cells, influencing immune responses and inflammation to elicit harmful or healing effects. This study focuses on the critical role of inflammation in heart disease progression and how non-coding RNAs in exosomes modulate the inflammatory process, either exacerbating or alleviating inflammation-related damage in the cardiovascular system.

Nanotechnology has revolutionized cancer therapy by introducing advanced drug delivery systems that enhance therapeutic efficacy while reducing adverse effects. By leveraging various nanoparticle platforms-including liposomes, polymeric nanoparticles, and inorganic nanoparticles-researchers have improved drug solubility, stability, and bioavailability. Additionally, new nanodevices are being engineered to respond to specific physiological conditions like temperature and pH variations, enabling controlled drug release and optimizing therapeutic outcomes. Beyond drug delivery, nanotechnology plays a crucial role in the theranostic field due to the functionalization of specific materials that combine tumor detection and targeted treatment features. This review analyzes the clinical impact of nanotechnology, spanning from early-phase trials to pivotal phase 3 studies that have obtained regulatory approval, while also offering a critical perspective on the preclinical domain and its translational potential for future human applications. Despite significant progress, greater attention must be placed on key challenges, such as biocompatibility barriers and the lack of regulatory standardization, to ensure the successful translation of nanomedicine into routine clinical practice.

Exosomes are extracellular vesicles that carry various biological substances and have potential as functional mediators in cancers. However, little is known about special molecules in colorectal cancer (CRC) exosomes and their immunological functions.

Using genomic data from the TCGA-CRC cohort, we constructed a prognostic model based on exosome-related lncRNA for the first time, and the biological role of MIR4713HG in CRC was deeply analyzed.

In this study, we downloaded the gene expression data and clinical data of CRC from the TCGA database. The limma package, SVM-REF and univariate Cox analysis were used to screen out core ERG (CERG) in CRC. LASSO and multivariate Cox regression analyses were used to filter out CERG-related LncRNA and construct a risk score. We explored the distribution and expression levels of ERG in immune cell types by scRNA-seq data. xCell was used to calculate the infiltration levels of stromal cells and immune cells in CRC. KM plotter was used for immunotherapy evaluation of core ERG. Next, we further provide colony formation assay, Transwell assay and xenograft models to understand the carcinogenic effect of MIR4713HG.

First, 43 differentially expressed ERG and 7 CERG were obtained. We explored the expression and distribution levels of CERG in 9 types of cells by scRNA-seq data. In addition, two key exosome-associated LncRNA (MIR4713HG and ZEB1-AS1) were obtained, and a risk score (EALncRI) was constructed. EALncRI could accurately predict the prognosis of CRC. Based on the EALncRI, we constructed a nomogram that is easy to use in clinical practice, which can more accurately and stably predict the prognosis of CRC patients. Furthermore, EALncRI was significantly correlated with the expression of 5 HLA molecules and 13 immune checkpoint molecules. MIR4713HG showed a good predictive effect in the overall survival of patients with immunotherapy evaluation. Knocking down the expression of MIR4713HG significantly inhibited proliferation and migration, and also impaired subcutaneous tumor growth in nude mice.

In this study, a variety of machine learning algorithms were used to construct the EALncRI based on ERG, which can effectively predict the prognosis and distinguish the immune landscape of CRC. More importantly, we conducted an in-depth study on MIR4713HG, which may become an important therapeutic target in CRC.

Ovarian cancer (OC) is the leading cause of gynecological cancer deaths. Current biomarkers of OC are not specific or sensitive enough. Extracellular vesicles (EVs), EV surface proteins and their cargo microRNA (miRNA) show potential as biomarkers. This study aimed to characterize the ability of EVs to identify early OC-biomarkers among blood donors six months before their diagnosis.

Study groups of OC patients, benign tumor patients (B), healthy blood donors (Control), and blood donors with incident OC diagnosis within six months of the last blood draw (Pre-diagnostic; PD) were established. Small EVs were enriched from plasma using ultracentrifugation. EVs were characterized by Dynamic Light Scattering (DLS), EV Array, NanoFlow Cytometry, Nanoparticle Tracking Analysis, and Western blots. RNA from EVs was isolated. A discovery study was performed on OC and B patients using the TaqMan Array Human MicroRNA A card. A validation study of 9 specific miRNAs was performed using RT-qPCR.

With DLS, it was identified that the OC patients' EVs were more heterogeneous in size compared to the other groups. Western blot identified CD63 and TSG101 in the EV enrichments. EV Array assessed 22 known protein biomarkers. TaqMan MicroRNA Array cards indicated a differential miRNA abundance between OC and B; however, technical replication and validation could not validate this pattern.

This study has analyzed EVs in OC, B, Control, and PD women. More extensive investigations of EV CD9, CD151, and CD81 in conjunction with other risk factors and well-known biomarkers like CA125 or HE4 should be the main objectives of future research.

Extracellular vesicles are nanoscale vesicles released by a diversity of cells that mediate intercellular communication by transporting an array of biomolecules. They are gaining increasing attention in cancer research due to their ability to carry specific biomarkers. This characteristic makes them potentially useful for highly sensitive, noninvasive diagnostic procedures and more precise prognostic assessments. Consequently, EVs are emerging as a transformative tool in cancer treatment, facilitating early detection and personalized medicine. Despite significant progress, clinical implementation is hindered by challenges in EV isolation, purification, and characterization. However, developing advanced biosensor technologies offers promising solutions to these obstacles. This review highlights recent progress in biosensors for EV detection and analysis, focusing on various sensing modalities including optical, electrochemical, microfluidic, nanomechanical, and biological sensors. We also explore techniques for EV isolation, characterization, and analysis, such as electron microscopy, atomic force microscopy, nanoparticle tracking analysis, and single-particle analysis. Furthermore, the review critically assesses the challenges associated with EV detection and put forward future directions, aiming to usher in a cutting-edge era of precision medicine through advanced, sensor-based, noninvasive early cancer diagnosis by detecting EV-carried biomarkers.

Doxorubicin (DOX) is the most effective chemotherapeutic for breast cancer, but it is usually associated with severe cardiotoxicity. Further investigation to alleviate its side effects is essential. The present study investigated the mechanism of the cross-organ communication between tumors and the heart and potential intervention targets. Morphological bubble-like protrusions were observed in both adult murine ventricular cardiomyocytes (AMVCs) and human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) cocultured with breast cancer cells (BCCs), along with elevated expression of pyroptosis-related proteins. Exosomes (EXOs) from DOX-treated BCCs aggravated DOX-induced cardiotoxicity (DOXIC) in an orthotopic mouse model of breast cancer. Blocking miRNAs by knocking down Rab27a or inhibiting the release of EXOs in cancer tissue by Dicer enzyme knockout attenuated this additional injury effect. Exosomal miRNA sequencing revealed that miR-216a-5p is especially upregulated in EXOs from DOX-induced BCCs. Mechanistically, miR-216a-5p was upregulated by enhanced transcription mediated by DOX-induced AMP-dependent transcription factor 3 (ATF3) and packaged into EXOs by splicing factor 3b subunit 4 (SF3B4) in BCCs. Itchy E3 ubiquitin-protein ligase (ITCH) was identified as a novel downstream target mRNA of miR-216a-5p. ITCH negatively mediated thioredoxin-interacting protein (TXNIP) ubiquitination to activate the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome pathway, ultimately leading to cardiomyocyte pyroptosis. Our findings revealed novel cross-organ pathogenic communication between breast cancer and the heart through the exosomal miR-216a-5p-mediated ITCH/TXNIP/NLRP3 pathway, which drives cardiomyocyte pyroptosis. These findings suggest that targeting myocardial miR-216a-5p or blocking harmful EXOs from breast cancer is a potential therapeutic strategy for alleviating DOXIC.

The increasing number of new cancer cases and cancer-related deaths worldwide highlights the urgent need to develop novel anti-tumor treatment methods to alleviate the current challenging situation. Nearly all organisms are capable of secreting extracellular vesicles (EVs), and these nano-scale EVs carrying biological molecules play an important role in intercellular communication, further affecting various physiological and pathological processes. Notably, EVs from different sources have differences in their characteristics and functions. Consequently, diverse EVs have been utilized as drug or vaccine delivery carriers for improving anti-tumor treatment due to their good safety, ease of modification and unique properties, and achieved satisfactory results. Meanwhile, the clinical trials of EV-based platform for tumor therapy are also continuously being conducted. Therefore, in this review, we summarize the recent research progress of EV-based tumor treatment methods, including the introduction of main sources and unique functions of EVs, the application of EVs in tumor treatment as well as their prospects and challenges. Additionally, considering the unique advantages of artificial EVs over natural EVs, we also highlighted their characteristics and applications in tumor treatments. We believe that this review will help researchers develop novel EV-based anti-tumor platforms through a bottom-up design and accelerate the development in this field.

Exosomes play an important role in the metastatic microenvironment, acting as a transmission belt that facilitates intercellular communication. By delivering proteins, nucleic acids, and other substances in the exosomes, they can change the function of the receptor target cells, change the microenvironment of the metastatic site, and promote the colonization of the tumor cells, thus promoting cancer metastasis. The interaction between tumor cells and the surrounding microenvironment is complex, with exosomes serving as key facilitators of crosstalk between the primary tumor microenvironment and the pre-metastasis microenvironment. Despite many current studies to explore exosomes, we still do not have a detailed understanding of the role and mechanism of exosomes in the pre-metastatic immune microenvironment, and there are many challenges in the clinical application of exosomes. In this paper, we summarize the role of exosomes in regulating the pre-metastatic immune microenvironment and its mechanism, focusing on how exosomes regulate the function of immune cells in the pre-metastatic microenvironment to promote tumor metastasis. In addition, the potential application of exosomes in tumor immunotherapy and strategies for targeting exosomes are discussed. This will contribute to the immunotherapy of cancer metastasis and promote the clinical application of exosomes.

Ferroptosis in the tumor microenvironment (TME) plays a crucial role in the development, metastasis, immune escape, and drug resistance of various types of cancer. A better understanding of ferroptosis in the TME could illuminate novel aspects of this process and promote the development of targeted therapies. Compelling evidence indicates that exosomes are key mediators in regulating the TME. In this respect, it is now understood that exosomes can deliver biologically functional molecules to recipient cells, influencing cancer progression by reprogramming the metabolism of cancer cells and their surrounding stromal cells through ferroptosis. In this review, we focus on the role of exosomes in the TME and describe how they contribute to tumor reprogramming, immunosuppression, and the formation of pre-metastatic niches through ferroptosis. In addition, we highlight exosome-mediated ferroptosis as a potential target for cancer therapy and discuss strategies employing exosomes in ferroptosis treatment. Finally, we outline the current applications and challenges of targeted exosome-mediated ferroptosis therapy in tumor immunotherapy and chemotherapy. Our aim is to advance research on the link between exosomes and ferroptosis in the TME, and we pose questions to guide future studies in this area.

Hepatocellular carcinoma (HCC) remains one of the major threats to human health worldwide. The emergence of systemic therapeutic options has greatly improved the prognosis of patients with HCC, particularly those with advanced stages of the disease. In this review, we discussed the pathogenesis of HCC, genetic alterations associated with the development of HCC, and alterations in the tumor immune microenvironment. Then, important indicators and emerging technologies related to the diagnosis of HCC are summarized. Also, we reviewed the major advances in treatments for HCC, offering insights into future prospects for next-generation managements.

With the advent of new therapeutic approaches, there is hope that anticancer treatment will eventually be possible without the use of chemotherapy. Efficient immunotherapeutic options have recently emerged in many cancers, offering a less aggressive approach, with overall better tolerance, making them also suitable for frail patients. Response to immunotherapy relies on the availability, functionality, and efficacy of the host's immune effector mechanisms. One of the key factors determining the efficacy of immunotherapy is the tumor microenvironment, which encompasses various immune effectors, including macrophages, which play a crucial role in regulating immune responses through phagocytosis and antigen presentation. Macrophages are prototypically divided, according to their polarization, into either the pro-inflammatory M1 type or the anti-inflammatory M2 type. In the tumor microenvironment, M2-polarized macrophages, known as tumor-associated macrophages (TAMs), are the predominant phenotype and are associated with tumor progression. The M1/M2 paradigm contributes to the understanding of tumor progression. Due to the variable microenvironment, the mechanisms regulating TAMs can vary across different cancers. Variations in TAM polarization may account for the different treatment responses in patients with similar diseases. This paper investigates the connection between TAMs, disease progression, and treatment responses in the most frequent solid hematologic cancer, diffuse large B-cell lymphoma.

Eukaryotes possess chromosome ends known as telomeres. As telomeres shorten, organisms age, a process defined as senescence. Although uncontrolled telomere lengthening has been naturally connected with cancer developments and immortalized state, many cancers are instead characterized by extremely short, genomically unstable telomeres that may hide cancer cells from immune attack. By contrast, other malignancies feature extremely long telomeres due to absence of 'shelterin' end cap protecting factors. The reason for rampant telomere extension in these cancers had remained elusive. Hence, while telomerase supports tumor progression and escape in cancers with very short telomeres, it is possible that different - transfer based or alternative - lengthening pathways be involved in the early stage of tumorigenesis, when telomere length is intact. In this Review, I hereby discuss recent discoveries in the field of telomeres and highlight unexpected links connecting cancer and telomere state. We hope these parallelisms may inform new therapies to eradicate cancers.

Cancer metastasis is a complicated biological process that critically affects cancer progression, patient outcomes, and treatment plans. A significant step in metastasis is the formation of a pre-metastatic niche (PMN). A small subset of cells within tumors, known as cancer stem cells (CSCs), possess unique characteristics including, differentiation into different cell types within the tumor, self-renewal, and resistance to conventional therapies, that enable them to initiate tumors and drive metastasis. PMN plays an important role in preparing secondary organs for the arrival and proliferation of CSCs, thereby facilitating metastasis. CSC-derived exosomes are crucial components in the complex interplay between CSCs and the tumor microenvironment. These exosomes function as transporters of various substances that can promote cancer progression, metastasis, and modulation of pre-metastatic environments by delivering microRNA (miRNA, miR) cargo. This review aims to illustrate how exosomal miRNAs (exo-miRs) secreted by CSCs can predispose PMN and promote angiogenesis and metastasis.

FOLFIRI, a combination of folinic acid, 5-fluorouracil, and irinotecan, is one of the recommended first-line chemotherapeutic treatments for metastatic colorectal cancer. Unfortunately, acquired FOLFIRI resistance represents a common obstacle in the treatment of metastatic colorectal cancer patients. Thus, we aimed to identify mechanisms, gene alterations, and gene expression signatures contributing to acquired FOLFIRI resistance by mimicking this problem in a cell culture model and subsequent translation in clinical data sets. Three FOLFIRI-resistant colorectal cancer (CRC) cell lines were established by continuous FOLFIRI treatment. Comparative mutation screening (161 genes) and transcriptomics (pathway and differential expression analyses) were performed in parental and resistant cells. Data reconciliation was performed in GSE62322, a clinical FOLFIRI responder data set (intrinsic resistance). Relapse-free survival (RFS) associations of identified differentially expressed genes and potential gene signatures were investigated in 8 clinical CRC data sets. No mutual genetic alterations were found in FOLFIRI-resistant derivatives. Resistant cell lines displayed activation of mitogen-activated protein kinase, immune response, and epithelial-mesenchymal transition pathways. Twelve differentially expressed genes, significantly differentially expressed in at least 2 of the 3 resistant cell lines, were identified. Comparison with GSE62322 and subsequent survival analyses revealed a 5-gene FOLFIRI signature comprised of CAV2, TNC, TACSTD2, SERPINE2, and PERP that was associated with RFS in multiple data sets including the cancer genome atlas CRC (hazard ratio [HR] =2.634, P = 4.53 × 10-6), in pooled samples of all data sets (all stages [N = 1981]: HR = 1.852, P = 6.44 × 10-13; stage IV [N = 260]: HR = 2.462, P = 5.22 × 10-9). A multivariate Cox regression analysis identified the 5-gene signature as an independent prognostic factor in the cancer genome atlas data set (HR = 1.89, P = .0202). Our analyses revealed a 5-gene FOLFIRI resistance signature associated with RFS that may help predict FOLFIRI resistance and thus avoid unnecessary ineffective treatment. Signature members might also represent targets to fight FOLFIRI resistance.

Extracellular vesicles (EVs) are small particles released by various cells, including cancer cells. They play a significant role in the development of different cancers, including brain metastasis. These EVs transport biomolecular materials such as RNA, DNA, and proteins from tumour cells to other cells, facilitating the spread of primary tumours to the brain tissue. EVs interact with the endothelial cells of the blood-brain barrier (BBB), compromising its integrity and allowing metastatic cells to pass through easily. Additionally, EVs interact with various cells in the brain's microenvironment, creating a conducive environment for incoming metastatic cells. They also influence the immune system within this premetastatic environment, promoting the growth of metastatic cells. This review paper focuses on the research regarding the role of EVs in the development of brain metastasis, including their impact on disrupting the BBB, preparing the premetastatic environment, and modulating the immune system. Furthermore, the paper discusses the potential of EVs as diagnostic and prognostic biomarkers for brain metastasis.

Exosomes are released by most cell types, including tumor-associated macrophages (TAMs), transfer diverse macromolecules and participate in intercellular communication in cancer. However, whether M2-polarized TAMs (M2-TAMs)-derived exosomes (M2-exos) transmit the oncogenic protein malate dehydrogenase 1 (MDH1) to reprogram lung adenocarcinoma (LUAD) cancer cells is unknown.

THP-1-differentiated macrophages were co-cultured with A549 cells to generate TAMs (M0-TAMs and M2-TAMs). Exosomes (M0-exos and M2-exos) were isolated from the co-culture supernatant and characterized. Xenograft studies were used to explore the effect of M2-exos-derived MDH1 on tumor growth. Expression analysis was performed by quantitative PCR, immunoblot and immunohistochemistry (IHC). Cell phenotype changes were detected by CCK-8, EdU, colony formation, wound-healing and transwell assays.

Bioinformatics analyses confirmed that MDH1 was overexpressed in human LUAD and high MDH1 expression was associated with poor prognosis. MDH1 depletion resulted in the in vitro suppression of LUAD cell growth, migration and invasiveness. M2-exos contained and transferred MDH1 into LUAD cells to upregulate MDH1 level in these cells. M2-exos-derived MDH1 enhanced the growth of A549 xenograft tumors in vivo and activated the Hippo/YAP pathway in vitro. Furthermore, Yes-associated protein (YAP) depletion could abrogate M2-exos-induced enhancements in these malignant phenotypes of A549 and HCC827 LUAD cells.

These findings demonstrate that exosomal MDH1 derived from M2-TAMs enhance LUAD cell growth and metastasis by activating the Hippo/YAP signaling, uncovering a novel exosomal mechanism of crosstalk between tumor microenvironment and LUAD cells.

Extracellular vesicles (EVs) have emerged as key cell-to-cell communication mediators and play significant roles in both physiological and pathological processes. In EVs, exosomes represent a distinct subpopulation of EVs that have been found to be involved in cancer initiation and therapeutic resistance. Exosomes transfer a diverse spectrum of molecular cargos that have significant effects on the tumor microenvironment (TME), thereby enabling cancer initiation, metastasis, and therapeutic resistance. Exosomes have recently been of interest in cancer therapy due to their role as important mediators of treatment resistance. The exosomal molecular content-proteins, miRNAs, and lncRNAs-allows exosomes to perform functions including drug efflux and detoxification, cell death pathway modulation, induction of epithelial-to-mesenchymal transition (EMT), and suppression of the immune system. In addition to facilitating immune and stromal cell interactions, exosomes cause extracellular matrix remodeling and induce tumor heterogeneity, making it more difficult to respond to therapy. This review covers intricate roles of exosomes in cancer therapy resistance with regard to their biogenesis, molecular content, and functional impact in the TME. Along with this, we also discuss new therapeutic strategies to overcome exosome-mediated resistance including utilizing exosome inhibitors, designed exosome therapy, and combination with conventional therapies. While exosomes hold promise in prediction and diagnosis through their biomarker function, their heterogeneous origins and cryptic functions make it difficult to target interventions. This review emphasizes that research on exosome-mediated pathways is urgently required to develop new therapeutic strategies that can improve cancer treatment outcomes.

Current therapeutic strategies for ischemic stroke fall short of the desired objective of neurological functional recovery. Therefore, there is an urgent need to develop new methods for the treatment of this condition. Exosomes are natural cell-derived vesicles that mediate signal transduction between cells under physiological and pathological conditions. They have low immunogenicity, good stability, high delivery efficiency, and the ability to cross the blood-brain barrier. These physiological properties of exosomes have the potential to lead to new breakthroughs in the treatment of ischemic stroke. The rapid development of nanotechnology has advanced the application of engineered exosomes, which can effectively improve targeting ability, enhance therapeutic efficacy, and minimize the dosages needed. Advances in technology have also driven clinical translational research on exosomes. In this review, we describe the therapeutic effects of exosomes and their positive roles in current treatment strategies for ischemic stroke, including their anti-inflammation, anti-apoptosis, autophagy-regulation, angiogenesis, neurogenesis, and glial scar formation reduction effects. However, it is worth noting that, despite their significant therapeutic potential, there remains a dearth of standardized characterization methods and efficient isolation techniques capable of producing highly purified exosomes. Future optimization strategies should prioritize the exploration of suitable isolation techniques and the establishment of unified workflows to effectively harness exosomes for diagnostic or therapeutic applications in ischemic stroke. Ultimately, our review aims to summarize our understanding of exosome-based treatment prospects in ischemic stroke and foster innovative ideas for the development of exosome-based therapies.

Exosomes are extracellular vesicles ranging from 40 to 100 nm in diameter that mediate intercellular communication by transferring proteins, lipids, nucleic acids, and other metabolites. In the context of cancer, exosomes influence the tumor microenvironment by carrying regulatory RNAs such as miRNA, circRNA, and lncRNA. They originate from various cells, including adipocytes, fibroblasts, and hepatocellular carcinoma (HCC) cells, and can either promote or inhibit cancer progression through pathways like MAPK and PI3K-Akt.

This review aims to explore the role of exosomes in the progression of solid cancers, emphasizing their self-induced activation mechanisms and how they modulate tumor behavior.

A comprehensive review of recent literature was conducted, focusing on studies that investigated the biological functions of exosomes in solid tumor progression, including their molecular cargo, cellular origin, and involvement in signaling pathways.

Findings from multiple studies indicate that cancer-derived exosomes contribute to tumor proliferation, metastasis, and therapy resistance by enhancing communication within the tumor microenvironment. These vesicles activate oncogenic pathways and can serve as biomarkers or therapeutic targets due to their role in disease modulation.

Exosomes play a pivotal role in solid cancer progression and offer significant potential in advancing our understanding of tumor biology. Their capacity to influence key signaling pathways and facilitate intercellular communication makes them promising candidates for novel diagnostic and therapeutic strategies.