Horticultural crops, including fruits, vegetables, flowers, and herbs, are essential for food security and economic sustainability. Advances in biotechnology, including genetic modification and omics approaches, have significantly improved these crops'traits. While initial transgenic efforts focused on protein-coding genes, recent research highlights the crucial roles of non-coding RNAs (ncRNAs) in plant growth, development, and gene regulation. ncRNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), influence key biological processes through transcriptional and post-transcriptional regulation. This review explores the classification, functions, and regulatory mechanisms of ncRNAs, emphasizing their potential in enhancing horticultural crop quality. This growing understanding offers promising avenues for enhancing crop performance and developing new horticultural varieties with improved traits. Additionally, we elucidate the role of ncRNA databases and predictive bioinformatics tools into modern horticultural crop improvement strategies.

Acute myeloid leukemia (AML) is the most common acute leukemia in adults and has the highest fatality rate. Patients aged 65 and above exhibit the poorest prognosis, with a mere 30 % survival rate within one year. One important issue in optimizing outcomes for AML patients is their limited ability to predict responses to specific therapies, response duration, and likelihood of relapse. Despite rigorous therapeutic interventions, a significant proportion of patients experience relapse. Consequently, there is a pressing need to introduce new targets for therapy. Sequencing and biotechnology have come a long way in the last ten years. This has made it easier for many omics technologies, like genomics, transcriptomics, proteomics, and metabolomics, to study molecular mechanisms of AML. An integrative approach is necessary to understand a complex biological process fully and offers an important opportunity to understand the information underlying diseases. In this review, we studied papers published between 2010 and 2024 employing omics approaches encompassing diagnosis, prognosis, and risk stratification of AML. Finally, we discuss prospects and challenges in applying -omics technologies to the discovery of novel biomarkers and therapy targets. Our review may be helpful for omics researchers who want to study AML from different molecular aspects.

Accumulated studies have demonstrated that long noncoding RNAs (lncRNAs) play crucial regulatory roles in diverse biological processes, such as embryonic development and cell differentiation. Comprehensive transcriptome analysis identifies extensive lncRNAs, gradually elucidating their functions across various contexts. Recent studies have highlighted the essential role of lncRNAs in definitive endoderm differentiation, underscoring their importance in early development. In this review, we have analyzed the features of overlapping, proximal, and desert lncRNAs, classified by genomic location, in pluripotent stem cells (PSCs) and the differentiation derivatives. Furthermore, we focus on the endoderm lineage and review the latest advancements in lncRNA identification and their distinct regulatory mechanisms. By consolidating current knowledge, we aim to provide a clearer perspective on how lncRNAs contribute to endoderm differentiation in different manners.

The objective was to assess the clinical efficacy of long non-coding RNA (lncRNA) alpha-2-macroglobulin-antisense 1 (A2M-AS1) in acute myocardial infarction (AMI).

One hundred patients with AMI and eighty patients with chest pain were recruited in the case-control study. A2M-AS1 expression was examined by quantitative real-time polymerase chain reaction (qRT-PCR). Receiver operating characteristic (ROC) analysis was utilized for evaluating the diagnostic value. Pearson's correlation analysis was used to analyze the correlation between A2M-AS1 and conventional AMI biomarkers. AMI-associated risk indicators were identified using logistic regression analysis.

A significant reduction of serum A2M-AS1 was measured in AMI patients relative to chest pain patients. A2M-AS1 had an area under the curve (AUC) of 0.927 to distinguish AMI patients from those with chest pain. Pearson's correlation analysis showed that A2M-AS1 was adversely correlated with white blood cell (WBC) (r=-0.6682, P < 0.001), low density lipoprotein cholesterol (LDL-C) (r=-0.5795, P < 0.001), creatine kinase MB (CK-MB) (r=-0.6022, P < 0.001) and cTnl (r=-0.5473; P < 0.001), while positively correlated with high density lipoprotein cholesterol (HDL-C) (r = 0.6445, P < 0.001). Relative to non-Major Adverse Cardiovascular Events (non-MACE) group, serum A2M-AS1 was obviously declined in the MACE group of AMI patients with high capacity to distinguish the MACE group from the non-MACE patients (AUC = 0.802). Additionally, A2M-AS1 (P = 0.013; OR = 0.268; 95%CI = 0.095-0.760) was a risk indicator for predicting MACE with AMI patients, as well as age (P = 0.014; OR = 3.478; 95%CI = 1.285-9.414).

A reduction in A2M-AS1 expression was observed in AMI patients, suggesting its potential as an underlying indicator for AMI diagnosis.

Hepatitis B virus (HBV) is a major global health concern, with maternal-fetal transmission being the primary route of transmission, which can lead to chronic HBV infection in newborns. Long non-coding RNAs (lncRNAs) play crucial roles in gene regulation and immune responses, but their involvement in HBV transmission during pregnancy remains unclear. This study aimed to assess the impact of tenofovir disoproxil fumarate (TDF)-based antiviral therapy on lncRNA expression profiles and immune signaling pathways in umbilical cord blood and placental tissues and to identify potential therapeutic targets for preventing intrauterine HBV infection.

Umbilical cord serum and placental tissues were collected from six HBV carriers. Three carriers received TDF-based antiviral therapy, and the remaining carriers who did not receive antiviral therapy served as controls. LncRNA microarray analysis and bioinformatics were used to evaluate the effects of antiviral therapy on lncRNA expression profiles and signaling pathways.

Antiviral therapy exerted minimal effects on lncRNA expression profiles in umbilical cord blood. In placental tissues, significant alterations in lncRNA expression profiles were observed, including 249 upregulated and 381 downregulated lncRNAs. Antiviral therapy activated innate immune pathways, such as intracellular DNA sensing, chemokine signaling, type I interferon, Jak-Stat, and interferon-γ-mediated adaptive immunity. Through intersection analysis, CPED1 was found differentially expressed in both cord blood and placental tissues. KEGG pathway analysis suggested that low CPED1 expression may inhibit virus transmission via the JAK-STAT pathway.

This study demonstrated that TDF-based antiviral therapy altered lncRNA expression and activated immune signaling pathways in placental tissues, offering insights into the molecular mechanisms of maternal-fetal HBV transmission.

Bladder cancer (BCa) is a prevalent urogenital malignancy, imposing a significant burden on health-care systems worldwide. Long noncoding RNAs (lncRNAs) are important regulators of carcinogenesis and affect BCa progression. In this study, the influence of lncRNA LINC00115 on malignant behavior of BCa cells were explored. Bioinformatics method was used for prediction of gene expression and downstream molecules of LIN00115. LINC00115 expression level in BCa cells was measured using RT-qPCR. After LINC00115 depletion, the proportion of viable, proliferative, and apoptotic BCa cells were calculated by methyl thiazolyl tetrazolium (MTT) assays, colony formation assays, and TUNEL staining, respectively. FISH was performed to verify the cellular distribution of LINC00115. The interaction between LINC00115 and miR-4701-5p and the binding between miR-4701-5p and P4HB were confirmed using RNA pulldown, RNA immunoprecipitation (RIP), and luciferase reporter assays. Experimental results showed that LINC00115 was highly expressed in BCa cells. The silencing of LINC00115 restrained BCa cell proliferation and stimulated apoptosis. LINC00115 could directly bind to miR-4701-5p and thus initiate P4HB upregulation in BCa cells. P4HB 3'untranslated region could be targeted by miR-4701-5p. Additionally, Amplification of P4HB expression offset the effects of LINC00115 knockdown on BCa cell proliferative and apoptotic behaviors. In conclusion, LINC00115 facilitates BCa cell growth and inhibits apoptosis via interaction with miR-4701-5p and upregulation of P4HB.

LncRNAs are RNA molecules of more than 200 nucleotides in length and participate in cellular metabolism and cellular responses through their diverse interactomedespite having no protein-coding capabilities. Such significant interactions also implicate the presence of lncRNAs in complex pathobiological pathways of various diseases, affecting cellular survival by modulating autophagy, inflammation and apoptosis. Proliferating cells harbour a complex microenvironment that mainly stimulate growth-specific activities such as DNA replication, repair, and protein synthesis. They also recognise damages at the macromolecular level, preventing them from reaching the next-generation. LncRNAs have shown significant association with the events occurring towards proliferation, regulating key events in dividing cells, and dysregulation of lncRNA transcriptome affects normal cellular life-cycle, promoting the development of cancer. Furthermore, lncRNAs also demonstrated an association with cancer growth and progression by regulating key pathways governing cell growth, epithelial-mesenchymal transition and metastasis. This makes lncRNAs an attractive target for the treatment of cancer and can also be used as a marker for the diagnosis and prognosis of diseases due to their differential expression in diseased samples. This review delves into the correlation of the lncRNA transcriptome with the fundamental cellular signalling and how this crosstalk shapes the complexity of the oncogenic microhabitat.

With the development of modern society and prolonged education, more women choose to delay their childbearing age, which greatly increases the number of women aged older than 35 years with childbearing needs. However, with increasing age, the quantity and quality of oocytes continue to fall, especially with increasing aneuploidy, which leads to a low in vitro fertilization (IVF) success rate, high abortion rate and high teratogenesis rate in assisted reproduction in women with advanced maternal age. In addition to genetics and epigenetics, follicular metabolism homeostasis is closely related to ovarian aging and oocyte aneuploidy. Glucose, lipid, and amino acid metabolism not only provide energy for follicle genesis but also regulate oocyte development and maturation. This review focuses on the relationships among follicular metabolism, oocyte aneuploidy, and ovarian aging and discusses potential therapeutic metabolites for ovarian aging.

Small nucleolar RNA host gene 10 (SNHG10) is a newly recognized long non-coding RNA (lncRNA) with significant implications in cancer biology. Abnormal expression of SNHG10 has been observed in various solid tumors and hematological malignancies. Research conducted in vivo and in vitro has revealed that SNHG10 plays a pivotal role in numerous biological processes, including cell proliferation, apoptosis, invasion and migration, drug resistance, energy metabolism, immune evasion, as well as tumor growth and metastasis. SNHG10 regulates tumor development through several mechanisms, such as competing with microRNA (miRNA) for binding sites, modulating various signaling pathways, influencing transcriptional activity, and affecting epigenetic regulation. The diverse biological functions and intricate mechanisms of SNHG10 highlight its considerable clinical relevance, positioning it as a potential pan-cancer biomarker and therapeutic target. This review aims to summarize the role of SNHG10 in tumorigenesis and cancer progression, clarify the molecular mechanisms at play, and explore its clinical significance in cancer diagnosis and prognosis prediction, along with its therapeutic potential.

Melanoma is the deadliest form of skin cancer, and its treatment poses significant challenges due to its aggressive nature and resistance to conventional therapies. Long non-coding RNAs (lncRNAs) represent a new frontier in the search for suitable targets to control melanoma progression and invasiveness. Indeed, lncRNAs exploit a wide range of regulatory functions along chromatin remodeling, gene transcription, post-transcription, transduction, and post-transduction to ultimately tune multiple cellular processes. The understanding of this intricate and flexible regulatory network orchestrated by lncRNAs in pathological conditions can strategically support the rational identification of promising targets, ultimately speeding up the setup of new therapeutics to integrate the currently available approaches. Here, the most recent findings on lncRNAs involved in melanoma will be analyzed. In particular, the functional links between their mechanisms of action and some frequently underestimated features, like their different subcellular localizations, will be highlighted.

The field of gene therapy using Adeno-associated viral (AAV) vector delivery is rapidly advancing in the biotherapeutics industry. Despite its successes, AAV manufacturing remains a challenge due to limited production yields. The triple plasmid transfection of HEK293 cells represents the most extensively utilized system for AAV production. The regulatory factors and mechanisms underlying viral production in HEK293 cells are largely unknown. In this study, we isolated high-titer AAV production clones from a parental HEK293 population using a single limiting dilution step, and subsequently elucidating their underlying molecular mechanisms through whole transcriptome analysis. LncRNA TCONS_00160397 was upregulated in clones and shown to promoted HEK293 cells proliferation and improved the titer of AAV production. Mechanistically, results from proteomics and metabolomics indicated that TCONS_00160397 regulated the ABC transporters pathway. These findings furnish a rich repository of knowledge and actionable targets for the rational optimization of HEK293-based producer lines, thereby paving the way for tangible improvements in AAV vector output and expediting the broad implementation of gene therapies.

Transcription takes place over a significant portion of the human genome. However, only a small portion of the transcriptome, roughly 1.2 %, consists of RNAs translated into proteins; the majority of transcripts, on the other hand, comprise a variety of RNA families with varying sizes and functions. A substantial portion of this diverse RNA universe consists of sequences longer than 200 bases, called the long non-coding RNA (lncRNA). The control of gene transcription, changes to DNA topology, nucleosome organization and structure, paraspeckle creation, and assistance for developing cellular organelles are only a few of the numerous tasks performed by lncRNA. The main focus of this study is on the function of lncRNA in controlling the levels and actions of cyclin-dependent kinase inhibitors (CDKIs). The enzymes required for the mitotic cycle's regulated progression are called cyclin-dependent kinases (CDKs). They have many degrees of regulation over their activities and interact with CDKIs as their crucial mechanisms. Interestingly, culminating evidence has clarified that lncRNAs are associated with several illnesses and use CDKI regulation to control cellular function. Nonetheless, despite the abundance of solid evidence in the literature, it still seems unlikely that lncRNA will have much of an impact on controlling cell proliferation or modulating CDKIs.

Atherosclerosis (AS) is a major contributor to cardiovascular diseases, characterized by high morbidity and mortality rates. Long non-coding RNAs (LncRNAs), as members of non-protein coding RNAs, play a crucial role in various biological processes that maintain homeostasis and influence disease progression. Research indicates that lncRNAs are involved in the pathogenesis of AS.

In this study, we aim to explore the role of lncRNAs in the pathogenesis of AS and the latest progress in the prevention and treatment of AS by targeted regulation of lncRNAs by traditional Chinese medicine (TCM), in order to provide more new beneficial targets for the treatment of AS and expand the application of TCM in the treatment of cardiovascular diseases.

The literature was retrieved, analyzed, and collected using PubMed, Web of Science, Sci-Hub, CNKI, Elsevier, ScienceDirect, SpringerLink, and Google Scholar. Search terms include "atherosclerosis", "traditional Chinese medicine", "natural products", "active ingredient", "lncRNAs", "herbal medicine", "cardiovascular diseases", "pharmacology", "toxicology", "clinical trials", etc., and several combinations of these keywords.

This study examines the primary mechanisms through which lncRNAs induce AS, such as dysfunction in endothelial cells, abnormal proliferation of vascular smooth muscle cells, cholesterol buildup in macrophages, formation of foam cells, inflammatory responses, and imbalances in lipid metabolism. Additionally, it summarizes 16 herbal monomers and 6 Chinese herbal compounds, along with an analysis of the toxicological aspects of TCM.

The study explores the existing approaches for modulating lncRNAs and emphasizes the significance and potential of herbal monomers, extracts, and formulations in this context.

This study aims to discover the role of lncRNA MIR17HG, referred to as MIR17HG, in cisplatin resistance for cholangiocarcinoma (CCA).

QRT-PCR was conducted to measure the expression of MIR17HG in cisplatin-resistant/sensitive CCA cells and clinical CCA specimens. Log-rank test was used to analyze the survival curve. Cck8-assay and flow cytometry were employed to detect the sensitivity of CCA cells to cisplatin and the apoptosis rate following different treatments, respectively. The next-generation sequencing was carried out to get gene transcripts after silencing MIR17HG in HCCC-9810 cells. The LncBase database was used to predict the target miRNA of MIR17HG, and MS2 RIP assay and dual luciferase assay were conducted to confirm their binding. MiRwalk database and the RNA sequencing data were utilized to screen the key genes regulated by MIR17HG/miR-138-5p axis and a dual luciferase assay was performed to confirm the binding site of miR-138-5p with AKAP9. Immunoblotting was further employed to give assistant evidence. Rescue experiments were performed to observe the function of miR-138-5p and AKAP9 in MIR17HG-induced cisplatin resistance.

MIR17HG overexpression predicts cisplatin resistance and poor prognosis in CCA. MIR17HG could bind with miR-138-5p to release AKAP9, thereby inhibiting cisplatin-induced apoptosis and promoting cisplatin resistance in CCA. MIR17HG silencing in CCA cells leads to expression alteration of genes, which are enriched in platinum resistance-related pathways.

LncRNA MIR17HG regulates platinum resistance-associated genes and promotes cisplatin resistance partially via the miR-138-5p/AKAP9 axis by inhibiting cisplatin-induced apoptosis in CCA.

The presence of the Hepatitis B virus (HBV) is considered as a valuable risk factor of hepatocellular carcinoma (HCC). To more deeply comprehend the molecular mechanism and transcriptome of HBV-induced HCC, we utilized tandem mass tagging (TMT)-based quantitative proteomics analysis and whole-transcriptome sequencing to analyze three sets of matched HepG2 hepatoma cells and HBV-positive HepAD38 cells. The differentially expressed (DE) proteins (1596), mRNAs (5263), miRNAs (581), lncRNAs (2672) and circRNAs (222) were subjected to differential expression and enrichment analyses in order to thoroughly assess the gene-regulatory circuits of HBV-induced HCC. Subsequently, the amounts of 321 DEproteins-DEmRNAs with common alterations were confirmed. According to functional pathway analysis, the DEproteins-DEmRNAs were primarily linked to signaling pathways, amino acid metabolism, and cellular function. Furthermore, the viability and significance of the ceRNA regulatory networks, LOC105377730/miR-4726-5p/FHL2 and hsa_circ_0001098/miR-2110/IGF2BP1, were randomly chosen and confirmed. Our work provides a valuable asset in terms of understanding regulatory activities at the RNA level, and might reveal fresh information about the fundamental mechanism and potential therapeutic targets of HBV-induced HCC.

Tongue squamous cell carcinoma (TSCC) is prevailing malignancy in the oral and maxillofacial region, characterized by its high frequency. LncRNA CCAT1 can promote tumorigenesis and progression in many cancers. Here, we investigated the regulatory mechanism by which CCAT1 influences growth and metastasis of TSCC. Levels of CCAT1, WTAP, TRIM46, PHLPP2, AKT, p-AKT, and Ki67 in TSCC tissues and cells were assessed utilizing qRT-PCR, Western blot and IHC. Cell proliferation, migration, and invasion were evaluated utilizing CCK8, colony formation, wound healing and transwell assays. Subcellular localization of CCAT1 was detected utilizing FISH assay. m6A level of CCAT1 was assessed using MeRIP. RNA immunoprecipitation (RIP), Co-immunoprecipitation (Co-IP) and RNA pull down elucidated binding relationship between molecules. Nude mouse tumorigenesis experiments were used to verify the TSCC regulatory function of CCAT1 in vivo. Metastatic pulmonary nodules were observed utilizing hematoxylin and eosin (HE) staining. CCAT1 silencing repressed TSCC cell proliferation, migration and invasion. Expression of CCAT1 was enhanced through N6-methyladenosine (m6A) modification of its RNA, facilitated by WTAP. Moreover, IGF2BP1 up-regulated CCAT1 expression by stabilizing its RNA transcript. CCAT1 bond to PHLPP2, inducing its ubiquitination and activating AKT signaling. CCAT1 mediated the ubiquitination and degradation of PHLPP2 by TRIM46, thereby promoting TSCC growth and metastasis. CCAT1/TRIM46/PHLPP2 axis regulated proliferation and invasion of TSCC cells, implying that CCAT1 would be a novel therapeutic target for TSCC patients.

Periodontitis is a multifactorial immune-mediated disease exacerbated by dysregulated alveolar bone homeostasis. Timely intervention is crucial for disease management to prevent tooth loss. To successfully manage periodontitis, it is imperative to understand the cellular and molecular mechanisms involved in its pathogenesis to develop novel treatment modalities. Non-surgical periodontal therapy (NSPT) such as subgingival instrumentation/debridement has been the underlying treatment strategy over the past decades. However, new NSPT approaches that target key signaling pathways regulating alveolar bone homeostasis have shown positive clinical outcomes. This narrative review aims to discuss endogenous bone homeostasis mechanisms impaired in periodontitis and highlight the clinical outcomes of preventive periodontal therapy to avoid invasive periodontal therapies. Although the anti-resorptive therapeutic adjuncts have demonstrated beneficial outcomes, adverse events have been reported. Diverse immunomodulatory therapies targeting the osteoblast/osteoclast (OB/OC) axis have shown promising outcomes in vivo. Future controlled randomized clinical trials (RCT) would help clinicians and patients in the selection of novel preventing therapies targeting key molecules to effectively treat or prevent periodontitis.

Long noncoding RNA (lncRNA) plays a critical role in cancer cell proliferation, invasion, metastasis, and chemoresistance. The current study introduces novel lncRNAs in colorectal cancer (CRC) through bioinformatics analysis. GSE134834 CRC-related microarray of Gene Expression Omnibus (GEO) was analyzed to identify differentially expressed genes (DEGs) in CRC samples against normal samples. Analysis revealed 6763 DEGs (p < 0.05 and |log fold change (FC)| ≥ 0.5) that include differentially expressed mRNA (DEmRNA) and differentially expressed long noncoding RNA (DElncRNA). Novel lncRNAs were identified, and to better understand the biological function of the identified lncRNAs, gene modules were constructed using weighted gene coexpression network analysis (WGCNA), and finally, two modules for lncRNAs were obtained. The coexpression modules with these lncRNAs were subjected to enrichment analysis in FunRich software to predict their functions through their coexpressed genes. Gene ontology results of modules related to novel lncRNA revealed they significantly enriched the cellular pathways regulation in cancer. The protein-protein interaction (PPI) network of novel lncRNAs-related modules was constructed using Search Tool for the Retrieval of Interacting Genes (STRING) and visualized using the Cytoscape software. Hub genes were screened from the PPI network by the CytoHubba plug-in of Cytoscape. The hub genes were MRTO4, CDK1, CDC20, RPF2, NOP58, NIFK, GTPBP4, BUB1, BUB1B, and BOP1 for the lightpink4 module and BYSL, RPS23 (ribosomal protein S23), RSL1D1 (ribosomal L1 domain containing 1), NAT10, NOP14, GNL2, MRPS12, NOL6 (nucleolar protein 6), IMP4, and RRP12 (ribosomal RNA processing 12 homolog) for the pink module. The expression levels of the top DEmRNA and module hub genes in CRC were validated using the Gene Expression Profiling Interactive Analysis (GEPIA) database. Generally, our findings offer crucial insight into the hub genes and novel lncRNAs in the development of CRC by bioinformatics analysis, information that may prove useful in the identification of new biomarkers and treatment targets in CRC; however, more experimental investigation is required to validate the findings of the present study.

Exosomes, as key mediators of intercellular communication, have been increasingly recognized for their role in the oncogenic processes, particularly in facilitating drug resistance. This article delves into the emerging evidence linking exosomal lncRNAs to the modulation of drug resistance mechanisms in cancers such as ovarian, cervical, and endometrial cancer. It synthesizes current research findings on how these lncRNAs influence cancer cell survival, tumor microenvironment, and chemotherapy efficacy. Additionally, the review highlights potential therapeutic strategies targeting exosomal lncRNAs, proposing a new frontier in overcoming drug resistance. By mapping the interface of exosomal lncRNAs and drug resistance, this article aims to provide a comprehensive understanding that could pave the way for innovative treatments and improved patient outcomes in female reproductive system cancers.

 Extremely preterm infants are at high risk of neonatal mortality and morbidity. Extreme preterm birth (PTB) may result from spontaneous preterm labor or preterm premature rupture of membranes or may be indicated due to preeclampsia, eclampsia, hypertension, or other causes. Our objective was to identify single nucleotide polymorphisms (SNPs) and biological pathways associated with spontaneous versus indicated extreme PTB using the neonatal genome.

 We evaluated 523 spontaneous births and 134 indicated births weighing 401 to 1,000 g at birth from the Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network's Genomics dataset by genome-wide association study (GWAS) and pathway analysis. The TOLSURF cohort was used to replicate the results.

 In the NRN GWAS, no statistically significant results were found, although the Manhattan plot showed one almost significant peak (rs60854043 on chromosome 14 at p = 1.03E-07) along with many other modest peaks at p = 1-9E-06, for a total of 15 suggestive associations at this locus. In the NRN pathway analysis, multiple pathways were identified, with the most significant being "GO_mf:go_low_density_lipoprotein_particle_receptor_activity" at p = 1.14E-06. However, these results could not be replicated in the TOLSURF cohort.

 Genomic differences are seen between infants born by spontaneous versus indicated extreme PTB. Due to the limited sample size, there is a need for larger studies.

· Genomic differences are seen between infants born by spontaneous versus indicated very PTB.. · Future studies with large sample sizes evaluating extreme PTB are necessary.. · Spontaneous PTB is more common than indicated extreme PTB..

Myasthenia gravis (MG) is an acquired autoimmune disease that is mediated by humoral immunity, supplemented by cellular immunity, along with participation of the complement system. The pathogenesis of MG is complex; although autoimmune dysfunction is clearly implicated, the specific mechanism remains unclear. Long non-coding RNAs (lncRNAs) are a class of non-coding RNA molecules with lengths greater than 200 nucleotides, with increasing evidence of their rich biological functions and high-level structure conservation. LncRNAs can directly interact with proteins and microRNAs to regulate the expression of target genes at the transcription and post-transcription levels. In recent years, emerging studies have suggested that lncRNAs play roles in the differentiation of immune cells, secretion of immune factors, and complement production in the human body. This suggests the involvement of lncRNAs in the occurrence and progression of MG through various mechanisms. In addition, the differentially expressed lncRNAs in peripheral biofluid may be used as a biomarker to diagnose MG and evaluate its prognosis. Moreover, with the development of lncRNA expression regulation technology, it is possible to regulate the differentiation of immune cells and influence the immune response by regulating the expression of lncRNAs, which will provide a potential therapeutic option for MG. Here, we review the research progress on the role of lncRNAs in different pathophysiological events contributing to MG, focusing on specific lncRNAs that may largely contribute to the pathophysiology of MG, which could be used as potential diagnostic biomarkers and therapeutic targets.

Obesity is attributed to a combination of factors such as lifestyle, environmental influences, and genetic background. Nowadays, the issue of obesity has grown to an epidemic scale. Environmental changes, having contributed to the sharp rise in obesity prevalence, are not the only contributing etiologic factors. Inherent biological variables interact with environmental factors resulting in obesity. Epigenetic mechanisms may explain part of obesity heritability. One of the recently discovered epigenetic mechanisms for controlling gene expression is long non-coding RNAs (lncRNAs). Circulating lncRNA p5549 and p19461 levels were reported to be significantly lower in individuals with obesity. This study aimed to evaluate whether weight loss following metabolic/bariatric surgery (MBS) can be related to altered expression levels of those lncRNAs, which have been reported to be reduced in individuals with obesity.

Comparison of circulating levels of lncRNA p5549 and p19461 before and 12 weeks after MBS in thirty-four patients was conducted to evaluate whether MBS can revert the altered levels of these lncRNAs. None of the participating patients were lost to follow-up, and all underwent re-evaluation of post-surgical expression levels.

lncRNA p5549 expression levels in serum were found to increase significantly in the postoperative samples compared to preoperative samples (fold increase: 4.63 ± 7.68, p = 0.014).

Epigenetic changes in patients with obesity, specifically lncRNA-p5549 expression levels, are reversed after MBS. The postoperative increase in the expression levels of lncRNA- p19461 was not statistically significant.

Transcription and RNA decay determine steady-state RNA levels in cells available for translation and RNA-mediated regulatory functions. Both processes can be assessed by various techniques, for majority, based on RNA labelling or chromatin immunoprecipitation, but require a high level of expertise. Here, we describe a cost-effective, fast, and simple protocol that enables the profiling of nascent and mature RNA in the cytoplasm, nucleoplasm, and chromatin through subcellular fractionation. The workflow can include α-amanitin inhibition of RNA Polymerase II to assess nascent RNAs as a proxy of transcriptional activity, or it can be used without this treatment to investigate distribution of partially processed or mature transcripts across distinct subcellular compartments. It is applicable for studying any of RNA biotypes, including small and long noncoding RNAs, mRNAs, and their splice variants, on both transcript-specific and transcriptome-wide scales. Nascent or mature RNAs isolated from each fraction can be further analyzed by any technique of choice (northern blot, reverse transcription, RNA sequencing).

To understand the transcriptomic profile of an individual cell in a multicellular organism, we must comprehend its surrounding environment and the cellular space where distinct molecular stimuli responses are located. Contradicting the initial perception that RNAs were nonfunctional and that only a few could act in chromatin remodeling, over the last few decades, research has revealed that they are multifaceted, versatile regulators of most cellular processes. Among the various RNAs, long non-coding RNAs (LncRNAs) regulate multiple biological processes and can even impact cell fate. In this sense, the subcellular localization of lncRNAs is the primary determinant of their functions. It affects their behavior by limiting their potential molecular partner and which process it can affect. The fine-tuned activity of lncRNAs is also tissue-specific and modulated by their cis and trans regulation. Hence, the spatial context of lncRNAs is crucial for understanding the regulatory networks by which they influence and are influenced. Therefore, predicting a lncRNA's correct location is not just a technical challenge but a critical step in understanding the biological meaning of its activity. Hence, examining these peculiarities is crucial to researching and discussing lncRNAs. In this review, we debate the spatial regulation of lncRNAs and their tissue-specific roles and regulatory mechanisms. We also briefly highlight how bioinformatic tools can aid research in the area.

1988 lncRNAs were identified in sweet sorghum roots under cadmium treatment; lncRNA 15962 and lncRNA 11558 were validated to be the key lncRNAs involved in regulating cadmium accumulation and translocation. Cadmium (Cd) has become one of the most harmful and widespread pollutants with industry development. Sweet sorghum is an ideal plant for phytoremediation of Cd-contaminated soil. However, little is known about the regulatory role of long non-coding RNAs (lncRNAs) associated with Cd stress response in sweet sorghum. Here, lncRNA-seq was carried out in the roots of two contrasting sweet sorghum genotypes (high-Cd accumulation genotype 'H18', and low-Cd accumulation genotype 'L69'). A total of 1988 lncRNAs were characterized, including 52 and 69 differentially expressed lncRNAs in 'H18' and 'L69' in response to Cd stress, respectively. Furthermore, the trans- or cis-target genes of lncRNAs were investigated. Then, 65 lncRNAs were characterized as the probable target of 117 miRNAs and 1888 genes were identified as putative cis-target genes of Cd-responsive lncRNAs. The dual-luciferase reporter assay indicated lncRNA 15962 may serve as the endogenous target mimics of sbi-miR5565e, which targeted two genes (Sobic.005G212900 and Sobic.009G144700) involved in cell wall metabolism. Four cis-target genes including SbYS1 which encoding a Cd chelate transporter, were up-regulated by overexpression of their corresponding lncRNAs in sweet sorghum protoplasts, suggesting the positive regulatory role of lncRNAs to these cis-target genes. Moreover, the expression of SbYS1 decreased when lncRNA 11558 was inhibited by exogenous miRNA application in 'H18' seedlings, further demonstrating the positive regulatory role of lncRNA 11558 to SbYS1. Altogether, our findings shed light on the regulatory role of lncRNAs associated with Cd accumulation and translocation in sweet sorghum.

Ferroptosis, a form of regulated cell death, has emerged as a crucial process in diverse pathophysiological states, encompassing cancer, neurodegenerative ailments, and ischemia-reperfusion injury. The glutathione (GSH)-dependent lipid peroxidation pathway, chiefly governed by glutathione peroxidase 4 (GPX4), assumes an essential part in driving ferroptosis. GPX4, as the principal orchestrator of ferroptosis, has garnered significant attention across cancer, cardiovascular, and neuroscience domains over the past decade. Noteworthy investigations have elucidated the indispensable functions of ferroptosis in numerous diseases, including tumorigenesis, wherein robust ferroptosis within cells can impede tumor advancement. Recent research has underscored the complex regulatory role of non-coding RNAs (ncRNAs) in regulating the GSH-GPX4 network, thus influencing cellular susceptibility to ferroptosis. This exhaustive review endeavors to probe into the multifaceted processes by which ncRNAs control the GSH-GPX4 network in ferroptosis. Specifically, we delve into the functions of miRNAs, lncRNAs, and circRNAs in regulating GPX4 expression and impacting cellular susceptibility to ferroptosis. Moreover, we discuss the clinical implications of dysregulated interactions between ncRNAs and GPX4 in several conditions, underscoring their capacity as viable targets for therapeutic intervention. Additionally, the review explores emerging strategies aimed at targeting ncRNAs to modulate the GSH-GPX4 pathway and manipulate ferroptosis for therapeutic advantage. A comprehensive understanding of these intricate regulatory networks furnishes insights into innovative therapeutic avenues for diseases associated with perturbed ferroptosis, thereby laying the groundwork for therapeutic interventions targeting ncRNAs in ferroptosis-related pathological conditions.

Long non-coding RNAs (lncRNAs) are importantly involved in the initiation and progression of non-small cell lung cancer (NSCLC). However, the classification and mechanisms of lncRNAs remain largely elusive.

Hence, we addressed this through bioinformatics analysis.

We utilized microarray technology to analyze lncRNAs and mRNAs in twenty paired NSCLC tumor tissues and adjacent normal tissues. Gene set enrichment analysis, Kyoto Encyclopedia of Genes and Genomes, and Gene Ontology were conducted to discern the biological functions of identified differentially expressed transcripts. Additionally, networks of lncRNA-mRNA co-expression, including cis-regulation, lncRNA-transcription factor (TF)-mRNA, trans-regulation, and lncRNA-miRNA-mRNA interactions were explored. Furthermore, the study examined differentially expressed transcripts and their prognostic values in a large RNA-seq dataset of 1016 NSCLC tumors and normal tissues extracted from the Cancer Genome Atlas (TCGA). The analysis revealed 391 lncRNAs and 344 mRNAs with differential expression in NSCLC tumor tissues compared to adjacent normal tissues. Subsequently, 43,557 co-expressed lncRNA-mRNA pairs were identified, including 27 lncRNA-mRNA pairs in cis, 9 lncRNA-TF-mRNA networks, 34 lncRNA-mRNA pairs in trans, and 8701 lncRNA-miRNA-mRNA competing endogenous RNA (ceRNA) networks. Notably, these lncRNAs were found to be involved in immune-related pathways. Six significant transcripts, including NTF4, PTPRD-AS, ITGA11, HID1-AS1, RASGRF2-AS1, and TBX2-AS1, were identified within the ceRNA network and trans-regulation.

This study brings important insights into the regulatory roles of lncRNAs in NSCLC, providing a fresh perspective on lncRNA research in tumor biology.

Over the past decade, regulatory non-coding RNAs (ncRNAs) produced by RNA Pol II have been revealed as meaningful players in various essential cellular functions. In particular, thousands of ncRNAs are produced at transcriptional regulatory elements such as enhancers and promoters, where they may exert multiple functions to regulate proper development, cellular programming, transcription or genomic stability. Here, we review the mechanisms involving these regulatory element-associated ncRNAs, and particularly enhancer RNAs (eRNAs) and PROMoter uPstream Transcripts (PROMPTs). We contextualize the mechanisms described to the processing and degradation of these short lived RNAs. We summarize recent findings explaining how ncRNAs operate locally at promoters and enhancers, or further away, either shortly after their production by RNA Pol II, or through post-transcriptional stabilization. Such discoveries lead to a converging model accounting for how ncRNAs influence cellular fate, by acting on transcription and chromatin structure, which may further involve factors participating to 3D nuclear organization.

LncRNAs are critical regulators of bladder cancer (BLCA), and ferroptosis is a newly discovered cell death responsible for mediating apoptosis and tumorigenesis. The present study aims to establish a prognostic signature of differentially expressed ferroptosis-related lncRNAs (DEFRlncRNAs) and explore the DEFRlncRNA associated with NUPR1 in BLCA.

DEFRlncRNAs in BLCA patients were screened using univariate and multivariate Cox and LASSO regression analyses. In vitro experiments were performed to detect the regulatory effects of DEFRlncRNAs on BLCA cells. A prognostic signature of DEFRlncRNAs in BLCA was created and validated. Moreover, we used RNA-binding protein immunoprecipitation (RIP) to evaluate the correlated DEFRlncRNA with NUPR1.

A prognostic signature involving 18 DEFRlncRNAs in BLCA was created. Overexpression of AL355353.2 or knockdown of AL136084.3 promoted apoptosis in 5637 and T24 cells in vitro. Results from Starbase database estimated that AL136084.3 was positively associated with NUPR1 (R = 0.229, p < 0.001). RIP analysis revealed the reciprocal binding of NUPR1 and AL136084.3 in BLCA.

The identified FRlncRNA pair signature has a good prognostic and clinical predictive value. The ferroptosis-related lncRNA AL136084.3 is correlated with NUPR1 in BLCA.

The aim of this study was to summarize the main findings of non-coding RNA (ncRNAs) in Turner syndrome (TS), correlating these biomolecules with the clinical manifestations in affected patients.

Searches were conducted in the databases of the United States National Library of Medicine (PubMed), Scientific Electronic Library Online (SciELO), and ScienceDirect, covering original English articles published from 2014 to 2023. Descriptors used included "lncRNAs and Turner Syndrome," "miRNAs and Turner Syndrome," and "circRNAs and Turner Syndrome." The studies that were included addressed the role of ncRNAs in the clinical characteristics of patients with TS. Exclusion criteria comprised texts in abstracts, reports, reviews, and monographs.

We identified 147 studies, of which seven were included. In the analysis of microRNAs, miR-486-5p and miR-320a stood out, being associated with ovarian development; miR-126-3p and miR-126-5p were related to greater aortic stiffness. Regarding long non-coding RNAs, the downregulation of XIST indicated dysfunctions in X chromosome inactivation. Concerning circular RNAs, circPPP2R3B, circCSF2RA, and circPCTN were related to immunological functions, while circ_0090421, circ_0090392, and circ_0089945 were linked to cardiac development.

The data from these studies demonstrate that these biomolecules play crucial roles in processes related to specific characteristics observed in TS patients. Besides being suggested as potential biomarkers, they may be useful in clinical practice.

Long non-coding RNAs (lncRNAs) have emerged as critical regulators of epigenome, modulating gene expression through DNA methylation, histone modification, and/or chromosome remodeling. Dysregulated lncRNAs act as oncogenes or tumor suppressors, driving tumor progression by shaping the cancer epigenome. By interacting with the writers, readers, and erasers of the epigenetic script, lncRNAs induce epigenetic modifications that bring about changes in cancer cell proliferation, apoptosis, epithelial-mesenchymal transition, migration, invasion, metastasis, cancer stemness and chemoresistance. This review analyzes and discusses the multifaceted role of lncRNAs in cancer pathobiology, from cancer genesis and progression through metastasis and therapy resistance. It also explores the therapeutic potential of targeting lncRNAs through innovative diagnostic, prognostic, and therapeutic strategies. Understanding the dynamic interplay between lncRNAs and epigenome is crucial for developing personalized therapeutic strategies, offering new avenues for precision cancer medicine.

The immunosuppressive tumor microenvironment (TME) is a prominent feature of glioblastoma (GBM), the most lethal primary brain cancer resistant to current immunotherapies. The mechanisms underlying GBM-TME remain to be explored. We report that long non-coding RNA (LncRNA) H19 encodes an immune-related protein called H19-IRP. Functionally separated from H19 RNA, H19-IRP promotes GBM immunosuppression by binding to the CCL2 and Galectin-9 promoters and activating their transcription, thereby recruiting myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs), leading to T cell exhaustion and an immunosuppressive GBM-TME. H19-IRP, overexpressed in clinical GBM samples, acts as a tumor-associated antigen (TAA) presented by major histocompatibility complex class I (MHC-I). A circular RNA vaccine targeting H19-IRP (circH19-vac) triggers a potent cytotoxic T cell response against GBM and inhibits GBM growth. Our results highlight the unrevealed function of H19-IRP in creating immunosuppressive GBM-TME by recruiting MDSCs and TAMs, supporting the idea of targeting H19-IRP with cancer vaccine for GBM treatment.

Oxaliplatin is a first-line chemotherapy drug for colorectal cancer (CRC), but many patients eventually lose treatment efficacy due to acquired resistance. AC105118.1 is a long non-coding RNA with unknown biological function. This research attempts to probe into the molecular regulatory mechanism of AC105118.1 in CRC oxaliplatin resistance.

The expression level of AC105118.1 in CRC tissues and cells was measured based on The Cancer Genome Atlas (TCGA) data and quantitative reverse transcription polymerase chain reaction (qRT-PCR). We utilized dual-luciferase assay and RNA immunoprecipitation to analyze the interaction between AC105118.1, miR-378a-3p, and their downstream target KIF26B. CCK-8, colony formation assay, and flow cytometry were employed to assess the half inhibitory concentration (IC50), cell proliferation, and apoptosis rate of HCT116/L-OHP cells treated with oxaliplatin. The glycolysis evaluation was completed by measuring the extracellular acidification rate (ECAR), glucose consumption, lactate production, and glycolysis-related proteins (HK2, GLUT1, and LDHA). TUNEL staining was used to detect the level of apoptosis.

AC105118.1 was specifically upregulated in CRC tissues and cells. AC105118.1 indirectly facilitated the expression of miRNA target gene KIF26B by sequestering miR-378a-3p. In HCT116/L-OHP cells, transfection with si-AC105118.1 resulted in a decrease in glycolysis level, a lower maximum IC50 required for oxaliplatin-treated cells, inhibited cell proliferation, and an increase in apoptosis rate. All of these effects were alleviated when simultaneously transfecting miR-378a-3p inhibitor or oe-KIF26B. Knockdown of AC105118.1 significantly inhibited oxaliplatin resistance to CRC in mice.

AC105118.1 facilitates glycolysis and increases CRC cells' resistance to oxaliplatin by targeting the miR-378a-3p/KIF26B axis. The present work shed new insights into the function and mechanism of AC105118.1 in molecular function and suggested that the AC105118.1/miR-378a-3p/KIF26B axis is a promising target for intervening CRC oxaliplatin resistance.

Exosomes, extracellular vesicles carrying a cargo rich in various non-coding RNAs (ncRNAs), have emerged as crucial mediators of intercellular communication. Their stability, abundance, and specificity make exosomal ncRNAs promising candidates for biomarker discovery. The discovery of exosomal ncRNAs has unveiled a novel avenue for the exploration of biomarkers in tumor early diagnosis. This review consolidates current knowledge on the role of exosomal ncRNAs as potential biomarkers in the early detection of various tumors. We provide an overview of recent studies demonstrating the diagnostic potential of exosomal ncRNAs across multiple cancer types, highlighting their sensitivity, specificity, and feasibility for early detection. This review underscores the potential of exosomal ncRNAs as non-invasive biomarkers for early tumor diagnosis, paving the way for improved clinical outcomes through timely intervention and personalized management strategies.

Type 2 diabetes mellitus (T2DM), a high-incidence chronic metabolic disorder, has emerged as a global health issue, where most patients need lifelong medication. Gaining insights into molecular mechanisms involved in T2DM development is expected to provide novel strategies for clinical prevention and treatment. Growing evidence validates that non-coding RNAs (ncRNAs) including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) function as crucial regulators in multiple biological processes of T2DM, inspiring various potential targets and drug candidates. In this review, we summarize the current understanding of ncRNA roles in T2DM and discuss the potential use of ncRNAs as targets and active molecules for drug discovery.

The role of long intergenic noncoding RNAs (lincRNAs) in fetal development has emerged as a significant area of study, challenging the traditional protein-centric view of gene expression. While messenger RNAs (mRNAs) have long been recognized for their role in encoding proteins, recent advances have illuminated the critical functions of lincRNAs in various biological processes. Initially identified through high-throughput sequencing technologies, lincRNAs are transcribed from intergenic regions between protein-coding genes and exhibit unique regulatory functions. Unlike mRNAs, lincRNAs are involved in complex interactions with chromatin and chromatin-modifying complexes, influencing gene expression and chromatin structure. LincRNAs are pivotal in regulating tissue-specific development and embryogenesis. For example, they are crucial for proper cardiac, neural, and reproductive system development, with specific lincRNAs being associated with organogenesis and differentiation processes. Their roles in embryonic development include regulating transcription factors and modulating chromatin states, which are essential for maintaining developmental programs and cellular identity. Studies using RNA sequencing and genetic knockout models have highlighted the importance of lincRNAs in processes such as cell differentiation, tissue patterning, and organ development. Despite their functional significance, the comprehensive annotation and understanding of lincRNAs remain limited. Ongoing research aims to elucidate their mechanisms of action and potential applications in disease diagnostics and therapeutics. This review summarizes current knowledge on the functional roles of lincRNAs in fetal development, emphasizing their contributions to tissue-specific gene regulation and developmental processes.

This research analyzes the potential of long non-coding RNAs (lncRNAs) as markers in determining the necessity of antiviral treatment in pregnant women by examining alterations in the expression profile of serum lncRNAs in pregnant women with elevated hepatitis B viral load (HBVL) under antiviral and non-antiviral treatment regimens between the second trimester and delivery.

Serum was obtained from 6 s-trimester pregnant women with high HBVL and no intrauterine infection. Then, 3 of these women were randomly selected for antiviral treatment, with the remaining 3 women undergoing non-antiviral treatment as control. Serum samples were again collected from these 6 women before delivery. The expression profile of lncRNAs was analyzed with microarray technology, followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. The axes of hub lncRNA-miRNA-mRNA were identified based on the competing endogenous RNA (ceRNA) network.

The expression profile of serum lncRNAs in pregnant women with high HBVL changed significantly from the second trimester of pregnancy until delivery under antiviral or non-antiviral treatment. The Venn diagram was utilized to screen out the jointly up-regulated and down-regulated lncRNAs in the serum of pregnant women under antiviral and non-antiviral treatment before delivery. Additionally, the KEGG pathway enrichment analysis results showed that lncRNAs might mediate the Hippo pathway in HBV infection. Based on the ceRNA network, 3 hub lncRNAs (CATG00000076041.1, LINC01310, and G014655) were found to potentially regulate the key gene TP73 in the Hippo pathway.

In this study, we retrieved co-differentially expressed lncRNAs in pregnant women with high HBVL under antiviral or non-antiviral treatment, which may be used as markers for evaluating whether pregnant women with high HBVL may be free of antiviral treatment. This study may provide a basis for preventing potential adverse effects of antiviral treatment on maternal and fetal health.

Osteoarthritis (OA) is the most common chronic joint degenerative disease. Herein, we investigated long non-coding RNA Opa-interacting protein 5-antisense transcript 1's (OIP5-AS1) in regulating mitophagy during OA.

RNA immunoprecipitation and RNA pull-down verified the relationship between molecules. Cell counting kit-8 detected cell viability. Enzyme-linked immunosorbent assay evaluated inflammatory cytokines secretion. Flow cytometry measured the contents of reactive oxygen species (ROS) and calcium. Immunofluorescence staining analysed TOMM20 and LC3B levels. JC-1 staining was adopted to measure mitochondrial membrane potential. The changes of mitophagy were analysed by transmission electron microscopy.

Lipopolysaccharide (LPS) treatment contributed to the decrease of chondrocyte viability, and calcium level and inhibited mitochondrial membrane potential, while elevating the secretion of inflammatory factors, ROS, and TOMM20 expression. OIP5-AS1 overexpression inhibited LPS-induced chondrocyte injury and activated mitophagy. OIP5-AS1 upregulated the peroxisome proliferator-activated receptor-γ (PPAR-γ) mRNA level to regulate adenosine monophosphate-activated protein kinase (AMPK)/v-akt murine thymoma viral oncogene homolog (Akt)/mammalian target of rapamycin (mTOR) signalling by interacting with FUS. PPAR-γ overexpression alleviated LPS-induced chondrocyte injury by activating AMPK/Akt/mTOR signalling. PPAR-γ knockdown reversed the promotion of OIP5-AS1 upregulation on mitophagy.

OIP5-AS1 promotes PPAR-γ expression to activate the AMPK/Akt/mTOR signalling, thereby enhancing mitophagy and alleviating OA progression.

ANRIL is known as a lncRNA that has many linear and circular isoforms and its polymorphisms are observed to be associated with the pathogenesis of many diseases including age-related diseases. Age-related diseases including atherosclerosis, ischemic heart disease, and Alzheimer's and Parkinson's disease are the most common cause of mortality in both developed and undeveloped countries and that is why a better understanding of their pathogenesis and underlying mechanisms is necessary for controlling their healthcare burden.In this review, we aim to gather the data of researches which have investigated the role of ANRIL in aging and its related diseases. The conclusions of this paper might give a new insight for decreasing the mortality rate of these diseases.

Platelets, produced by megakaryocytes, play unique roles in physiological processes, such as hemostasis, coagulation, and immune regulation, while also contributing to various clinical diseases. During megakaryocyte differentiation, the morphology and function of cells undergo significant changes due to the programmed expression of a series of genes. Epigenetic changes modify gene expression without altering the DNA base sequence, effectively affecting the inner workings of the cell at different stages of growth, proliferation, differentiation, and apoptosis. These modifications also play important roles in megakaryocyte development and platelet biogenesis. However, the specific mechanisms underlying epigenetic processes and the vast epigenetic regulatory network formed by their interactions remain unclear. In this review, we systematically summarize the key roles played by epigenetics in megakaryocyte development and platelet formation, including DNA methylation, histone modification, and non-coding RNA regulation. We expect our review to provide a deeper understanding of the biological processes underlying megakaryocyte development and platelet formation and to inform the development of new clinical interventions aimed at addressing platelet-related diseases and improving patients' prognoses.

Human endogenous retroviruses (HERVs) are widely recognized as the result of exogenous retroviruses infecting the ancestral germline, stabilizing integration and vertical transmission during human genetic evolution. To date, endogenous retroviruses (ERVs) appear to have been selected for human physiological functions with the loss of retrotransposable capabilities. ERV elements were previously regarded as junk DNA for a long time. Since then, the aberrant activation and expression of ERVs have been observed in the development of many kinds of human diseases, and their role has been explored in a variety of human disorders such as cancer. The results show that specific ERV elements play respective crucial roles. Among them, long non-coding RNAs (lncRNAs) transcribed from specific long-terminal repeat regions of ERVs are often key factors. lncRNAs are over 200 nucleotides in size and typically bind to DNA, RNA, and proteins to perform biological functions. Dysregulated lncRNAs have been implicated in a variety of diseases. In particular, studies have shown that the aberrant expression of some ERV-derived lncRNAs has a tumor-suppressive or oncogenic effect, displaying significant functional bidirectionality. Therefore, theses lncRNAs have a promising future as novel biomarkers and therapeutic targets to explore the concise relationship between ERVs and cancers. In this review, we first summarize the role of ERV-derived lncRNAs in physiological regulation, mainly including immunomodulation, the maintenance of pluripotency, and erythropoiesis. In addition, pathological regulation examples of their aberrant activation and expression leading to carcinogenesis are highlighted, and specific mechanisms of occurrence are discussed.

Cancer treatment has long been fraught with challenges, including drug resistance, metastasis, and recurrence, making it one of the most difficult diseases to treat effectively. Traditional therapeutic approaches often fall short due to their inability to target cancer stem cells and the complex genetic and epigenetic landscape of tumors. In recent years, cancer immunotherapy has revolutionized the field, offering new hope and viable alternatives to conventional treatments. A particularly promising area of research focuses on non-coding RNAs (ncRNAs), especially long non-coding RNAs (lncRNAs), and their role in cancer resistance and the modulation of signaling pathways. To address these challenges, we performed a comprehensive review of recent studies on lncRNAs and their impact on cancer immunotherapy. Our review highlights the crucial roles that lncRNAs play in affecting both innate and adaptive immunity, thereby influencing the outcomes of cancer treatments. Key observations from our review indicate that lncRNAs can modify the tumor immune microenvironment, enhance immune cell infiltration, and regulate cytokine production, all of which contribute to tumor growth and resistance to therapies. These insights suggest that lncRNAs could serve as potential targets for precision medicine, opening up new avenues for developing more effective cancer immunotherapies. By compiling recent research on lncRNAs across various cancers, this review aims to shed light on their mechanisms within the tumor immune microenvironment.