Cervical cancer (CC) is a global public health concern, primarily caused by persistent infection with oncogenic types of human papillomavirus (HPV). The World Health Organization (WHO) has established a plan to eliminate CC as a public health issue by the year 2100. However, the implementation of the HPV vaccine is impeded by vaccine restrictions and misinformation despite its demonstrated effectiveness. The CC treatment is influenced by the disease stage, with an unfavorable prognosis for those in advanced stages. This study aimed to investigate the potential of long non-coding RNAs (lncRNAs) in CC by identifying and characterizing related lncRNAs, elucidating their regulatory mechanisms and molecular interactions, and analyzing their expression patterns in patients with diverse responses to chemoradiotherapy. Non-stem cells from CC were isolated using flow cytometry sorting and used for total RNA extraction. The RNA was used to build libraries that were subsequently sequenced using the Illumina Nextseq 550.417 lncRNAs that showed differentially expressed between CC patients who responded or not to treatment. Further analysis demonstrated that these lncRNAs significantly interact with several molecules, which play crucial roles in CC progression and therapeutic resistance. Statistical analysis correlated the expression profile of these lncRNAs with treatment efficacy. Three lncRNAs, ENSG00000267838, ENSG00000266340, and FRMD6-AS1, were identified with positive expression related to non-response to chemoradiotherapy and worse progression-free survival in CC patients. Specifically, lncRNA ENSG00000267838 has its up-regulation related to non-response and down-regulation to response to chemoradiotherapy treatment.

Oral cancer (OC) ranks among the most prevalent head and neck cancers, becoming the eleventh most common cancer worldwide with ~350,000 new cases and 177,000 fatalities annually. The rising trend in the occurrence of OC among young individuals and women who do not have tobacco habits is escalating rapidly. Surgical procedures, radiation therapy, and chemotherapy are among the most prevalent treatment options for oral cancer. To achieve better therapy and an early detection of the cancer, it is essential to understand the disease's etiology at the molecular level. Saliva, the most prevalent body fluid obtained non-invasively, holds a collection of distinct non-coding RNA pools (ncRNAomes) that can be assessed as biomarkers for identifying oral cancer. Non-coding signatures, which are transcripts lacking a protein-coding function, have been identified as significant in the progression of various cancers, including oral cancer. This review aims to examine the role of various salivary ncRNAs (microRNA, circular RNA, and lncRNA) associated with disease progression and to explore their functions as potential biomarkers for early disease identification to ensure better survival outcomes for oral cancer patients.

Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasm in which all the patients has the translocation (9;22) that generates de BCR::ABL1 tyrosine kinase. Despite this disease possessing a good biomarker (BCR::ABL1 transcripts level) for diagnosis and prognosis, many studies has been performed to investigate other molecules, such as the long noncoding RNAs (lncRNAs) and mRNAs, as potential biomarkers with the aim of predicting a change in BCR::ABL1 levels and as an associated biomarker. A RNAseq was performed comparing 6 CML patients with high BCR::ABL1 expression with 6 healthy control individuals, comprising the investigation cohort to investigate these molecules. To validate the results obtained by RNAseq, samples of 87 CML patients and 42 healthy controls were used in the validation cohort by RT-qPCR assays. The results showed lower expression of HOTAIR and PTGS2 in CML patients. The HOTAIR expression is inversely associated with BCR::ABL1 expression in imatinib-treated CML patients, and to PTGS2 showing that CML patients with high BCR::ABL1 expression showed reduced PTGS2 expression.

The characteristics of a tumor are largely determined by its interaction with the surrounding micro-environment (TME). TME consists of both cellular and non-cellular components. Cancer-associated fibroblasts (CAFs) are a major component of the TME. They are a source of many secreted factors that influence the survival and progression of tumors as well as their response to drugs. Identification of markers either overexpressed in CAFs or unique to CAFs would pave the way for novel therapeutic strategies that in combination with conventional chemotherapy are likely to have better patient outcome.

Fibroblasts have been derived from Benign Prostatic Hyperplasia (BPH) and prostate cancer. RNA from these has been used to perform a transcriptome analysis in order to get a comparative profile of normal and cancer-associated fibroblasts.

The study has identified 818 differentially expressed mRNAs and 17 lincRNAs between normal and cancer-associated fibroblasts. Also, 15 potential lincRNA-miRNA-mRNA combinations have been identified which may be potential biomarkers.

This study identified differentially expressed markers between normal and cancer-associated fibroblasts that would help in targeted therapy against CAFs/derived factors, in combination with conventional therapy. However, this would in future need more experimental validation.

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.

Myocardial infarction (MI) stands at top global causes of death in developed countries, owing mostly to atherosclerotic plaque growth and endothelial injury-induced reduction in coronary blood flow. While early reperfusion techniques have improved outcomes, long-term treatment continues to be difficult. The function of lncRNAs extends to regulating gene expression in various conditions, both physiological and pathological, such as cardiovascular diseases. The objective of this research is to extensively evaluate the significance of the lncRNA called Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in the development and management of MI. According to research, MALAT1 is implicated in processes such as autophagy, apoptosis, cell proliferation, and inflammation in the cardiovascular system. This investigation examines recent research examining the effects of MALAT1 on heart function and its potential as a mean of diagnosis and treatment for post- MI complications and ischemic reperfusion injury.

In recent years, long non-coding RNAs (lncRNAs) have emerged as potential regulators of biological processes and genes, with the potential to serve as valuable biomarkers for cancer diagnosis and prognosis prediction. This work proposes an evolutionary learning-based method, EL-COAD, to identify a robust lncRNA signature with biomarker discovery for predicting stages of colon adenocarcinoma (COAD). The COAD patient cohorts were obtained from both the Cancer Genome Atlas and Gene Expression Omnibus (gse17536) databases. EL-COAD incorporates a bi-objective combinatorial genetic algorithm with a support vector machine for selecting a minimal number of lncRNAs while maximizing prediction accuracy. EL-COAD identified a 15-lncRNA signature and achieved a five-fold cross-validation and area under receiver operating characteristic curve of 79.4% and 0.792, respectively. Utilising the 10 lncRNAs from the signature for an independent dataset gse17536, the Sequential Minimal Optimization model achieved a test accuracy of 64.15%. Furthermore, the lncRNAs of the signature were prioritized, with the top five being TMEM105, DUXAP8, APCDD1L-DT, PCAT6, and a novel transcript, ENSG00000226308. Furthermore, both Kyoto Encyclopedia of Genes and Genomes pathway and Disease Ontology analyses provided strong support for the viability of this model-independent signature, emphasising ENSG00000226308 as a promising biomarker.

The plant long noncoding (lnc)RNA field is on the brink of transitioning from large-scale identification of lncRNAs to their functional characterization. Due to the cross-kingdom conservation of interaction types and molecular functions, there is much to be learned from mammalian lncRNA research. Here, we discuss the different molecular processes involving lncRNAs from the regulation of chromatin to splicing. Furthermore, we discuss the lncRNA interactome, which includes proteins, other RNAs, and DNA. We explore and discuss how mammalian lncRNA functionalities could be reflected in similar pathways in plants and hypothesize that several breakthroughs in mammalian research could lead to the discovery of novel plant lncRNA molecular functions. Expanding our knowledge of the biological role of lncRNAs and their multiple applications paves the way for future agricultural applications.

Many types of gynecological cancer (GC) are often silent until they reach an advanced stage, and are therefore often diagnosed too late for effective treatment. Hence, there is a real need for more efficient diagnosis and treatment for patients with GC. During recent years, researchers have increasingly studied the impact of microRNAs cancer development, leading to a number of applications in detection and treatment. MicroRNAs are a particular group of tiny RNA molecules that regulate regular gene expression by affecting the translation process. The downregulation of numerous miRNAs has been observed in human malignancies. Let-7 is an example of a miRNA that controls cellular processes as well as signaling cascades to affect post-transcriptional gene expression. Recent research supports the hypothesis that enhancing let-7 expression in those cancers where it is downregulated may be a potential treatment option. Exosomes are tiny vesicles that move through body fluids and can include components like miRNAs (including let-7) that are important for communication between cells. Studies proved that exosomes are able to enhance tumor growth, angiogenesis, chemoresistance, metastasis, and immune evasion, thus suggesting their importance in GC management.

Inflammatory bowel disease (IBD) is a group of recurrent chronic inflammatory diseases, including Crohn's disease (CD) and ulcerative colitis (UC). Although IBD has been extensively studied for decades, its cause and pathogenesis remain unclear. Existing research suggests that IBD may be the result of an interaction between genetic factors, environmental factors and the gut microbiome. IBD is closely related to non-coding RNAs (ncRNAs). NcRNAs are composed of microRNA(miRNA), long non-coding RNA(lnc RNA) and circular RNA(circ RNA). Compared with miRNA, the role of lnc RNA in IBD has been little studied. Lnc RNA is an RNA molecule that regulates gene expression and regulates a variety of molecular pathways involved in the pathbiology of IBD. Targeting IBD-associated lnc RNAs may promote personalized treatment of IBD and have therapeutic value for IBD patients. Therefore, this review summarized the effects of lnc RNA on the intestinal epithelial barrier, inflammatory response and immune homeostasis in IBD, and summarized the potential of lnc RNA as a biomarker of IBD and as a predictor of therapeutic response to IBD in the future.

Rapid proliferation and metastasis of breast cancer contributed to poor clinical prognosis. Accumulating evidence revealed that the dysregulation of long noncoding RNAs (lncRNAs) was associated with breast cancer progression. However, the role of lncRNA DLG5-AS1 in breast cancer has not been established. Here, we investigated the mechanisms of DLG5-AS1 in the development of breast cancer. We found that the expression of DLG5-AS1 was significantly upregulated in breast cancer tissues and cell lines. DLG5-AS1 interference markedly restrained AU565 cell proliferation, invasion, the expression of apoptosis related (caspase3 and caspase8) and Wnt/β-catenin pathway related proteins (wnt5a, β-Catenin and c-Myc), as well as promoted cell apoptosis, whereas DLG5-AS1 overexpression showed an opposite effects. In addition, DLG5-AS1 could directly bind with miR-519 b-3p. We also found that enhancer of zeste homolog 2 (EZH2) is a direct target of miR-519 b-3p, and DLG5-AS1 upregulated EZH2 expression by inhibiting the expression of miR-519 b-3p. EZH2 restrained secreted frizzled related protein 1 (SFRP1) expression through inducing H3 histone methylation in its promoter. MiR-519 b-3p overexpression or SFRP1 knockdown memorably reversed the effects of DLG5-AS1 overexpression on cell functions and Wnt/β-Catenin pathway related protein expression. Finally, in vivo experiments demonstrated that silencing of DLG5-AS1 inhibited xenograft tumor development in mice. Taken together, these findings demonstrated that DLG5-AS1 facilitated cell proliferation and invasion by promoting EZH2-mediated transcriptional silencing of SFRP1 in breast cancer.

A growing number of studies have suggested the involvement of long non-coding RNAs as the key players in not just the initiation and progression of the tumor microenvironment, but also in chemotherapy tolerance. In the present study, generated 5-FU-resistant SW480/DR cells were analyzed via cDNA microarray for its aberrant lncRNAs and mRNAs expression in comparison with the 5-FU-susceptible SW480/DS cells. Among the 126 lncRNAs described, lncRNAs GNAS-AS1, MIR205HG, and LOC102723721 have been identified to be significantly upregulated, while lncRNs lnc-RP11-597K23.2.1-2, LOC100507639, and CCDC144NL-AS1 have been found to be significantly downregulated. In the meantime, bioinformatic analysis through gene ontology studies of aberrantly expressed mRNAs revealed "regulated exocytosis", among others, as the biological process most impacted in SW480/DR cells. To investigate, exosome purification was then carried out and its characterization were validated via transmission electron microscopy and nanoparticle tracking analysis. Interestingly, it was determined that the 5-FU-resistant SW480/DR cells secretes significantly higher concentration of extracellular vesicles, particularly, exosomes when compared to the 5-FU-susceptible SW480/DS cells. Based on the lncRNA-mRNA interaction network analysis generated, lncRNA GNAS-AS1 and MIR205HG have been identified to be potentially involved in the incidence of 5-FU resistance in SW480 colon cancer cells through promoting increased release of exosomes into the intercellular matrix. Our study hopes not only to provide insights on the list of involved candidate lncRNAs, but also to elucidate the role exosomes play in the initiation and development of 5-FU chemotherapy resistance in colon cancer cells.

The long noncoding RNAs (lncRNAs) comprise a wide range of RNA species whose length exceeds 200 nucleotides, which regulate the expression of genes and cellular functions in a wide range of organisms. Several diseases, including malignancy, have been associated with lncRNA dysregulation. Due to their functions in cancer development and progression, lncRNAs have emerged as promising biomarkers and therapeutic targets in cancer diagnosis and treatment. Several studies have investigated the anti-cancer properties of lncRNAs; however, only a few lncRNAs have been found to exhibit tumor suppressor properties. Furthermore, their length and poor stability make them difficult to synthesize. Thus, to overcome the instability of lncRNAs, poor specificity, and their off-target effects, researchers have constructed nanocarriers that encapsulate lncRNAs. Recently, translational medicine research has focused on delivering lncRNAs into tumor cells, including cancer cells, through nano-drug delivery systems in vivo. The developed nanocarriers can protect, target, and release lncRNAs under controlled conditions without appreciable adverse effects. To deliver lncRNAs to cancer cells, various nanocarriers, such as exosomes, microbubbles, polymer nanoparticles, 1,2-dioleyl-3-trimethylammoniumpropane chloride nanocarriers, and virus-like particles, have been successfully developed. Despite this, every nanocarrier has its own advantages and disadvantages when it comes to delivering nucleic acids effectively and safely. This article examines the current status of nanocarriers for lncRNA delivery in cancer therapy, focusing on their potential to enhance cancer treatment.

Non-coding RNAs (ncRNAs), generated from nonprotein coding DNA sequences, constitute 98-99% of the human genome. Non-coding RNAs encompass diverse functional classes, including microRNAs, small interfering RNAs, PIWI-interacting RNAs, small nuclear RNAs, small nucleolar RNAs, and long non-coding RNAs. With critical involvement in gene expression and regulation across various biological and physiopathological contexts, such as neuronal disorders, immune responses, cardiovascular diseases, and cancer, non-coding RNAs are emerging as disease biomarkers and therapeutic targets. In this review, after providing an overview of non-coding RNAs' role in cell homeostasis, we illustrate the potential and the challenges of state-of-the-art computational methods exploited to study non-coding RNAs biogenesis, function, and modulation. This can be done by directly targeting them with small molecules or by altering their expression by targeting the cellular engines underlying their biosynthesis. Drawing from applications, also taken from our work, we showcase the significance and role of computer simulations in uncovering fundamental facets of ncRNA mechanisms and modulation. This information may set the basis to advance gene modulation tools and therapeutic strategies to address unmet medical needs.

Understanding the intricate molecular mechanisms governing the fate of human adipose-derived stem cells (hASCs) is essential for elucidating the delicate balance between adipogenic and osteogenic differentiation in both healthy and pathological conditions. Long non-coding RNAs (lncRNAs) have emerged as key regulators involved in lineage commitment and differentiation of stem cells, operating at various levels of gene regulation, including transcriptional, post-transcriptional, and post-translational processes. To gain deeper insights into the role of lncRNAs' in hASCs' differentiation, we conducted a comprehensive analysis of the lncRNA transcriptome (RNA-seq) and translatome (polysomal-RNA-seq) during a 24 h period of adipogenesis and osteogenesis. Our findings revealed distinct expression patterns between the transcriptome and translatome during both differentiation processes, highlighting 90 lncRNAs that are exclusively regulated in the polysomal fraction. These findings underscore the significance of investigating lncRNAs associated with ribosomes, considering their unique expression patterns and potential mechanisms of action, such as translational regulation and potential coding capacity for microproteins. Additionally, we identified specific lncRNA gene expression programs associated with adipogenesis and osteogenesis during the early stages of cell differentiation. By shedding light on the expression and potential functions of these polysome-associated lncRNAs, we aim to deepen our understanding of their involvement in the regulation of adipogenic and osteogenic differentiation, ultimately paving the way for novel therapeutic strategies and insights into regenerative medicine.

Alveolar echinococcosis is a severe zoonotic disease caused by the pseudotumoral intrahepatic development of the larval stage of the tapeworm Echinococcus multilocularis. The diagnosis of alveolar echinococcosis is hard since it has features of liver cancer. LncRNAs are among the non-coding RNAs that have received the most attention in recent biomarker studies. Here, we aimed to identify the serum-derived exosomal lncRNAs associated with alveolar echinococcosis in humans with RNA-seq. After RNA isolation from exosomes, we performed RNA-seq to determine the lncRNAs. We found 8 target genes in the cis direction and a total of 6468 gene targets for lncRNAs were identified in the trans direction. Totally 621 mRNA transcripts were found as differentially expressed between the controls and patients. 278 of them were up-regulated and 343 were down-regulated. Moreover, 234 lncRNAs were found as differentially expressed between the controls and patients. 58 of them were up-regulated, and 176 of them were down-regulated. The top five biological pathways regulated by identified lncRNAs were detected in this study. As a result, it is thought that these results will contribute to lncRNA-based biomarker studies that can be used in the early diagnosis of alveolar echinococcosis in humans.

LINC00941, also known as lncRNA-MUF, is an intergenic non-coding RNA located on chromosome 12p11.21. It actively participates in a complex competing endogenous RNA network, regulating the expression of microRNA and its downstream proteins. Through transcriptional and post-transcriptional regulation, LINC00941 plays a vital role in multiple signaling pathways, influencing cell behaviors such as tumor cell proliferation, epithelial-mesenchymal transition, migration, and invasion. Noteworthy is its consistently high expression in various tumor types, closely correlating with clinicopathological features and cancer prognoses. Elevated LINC00941 levels are associated with adverse clinical outcomes, including increased tumor size, extensive lymphatic metastasis, and distant metastasis, leading to poorer survival rates across different cancers. Additionally, LINC00941 and its associated genes are linked to various targeted drugs available in the market. In this comprehensive review, we systematically summarize existing studies, detailing LINC00941's differential expression, clinicopathological and prognostic implications, regulatory mechanisms, and associated therapeutic drugs. Our analysis includes relevant charts and incorporates bioinformatics analyses to verify LINC00941's differential expression in pan-cancer and explore potential transcriptional regulation patterns of downstream targets. This work not only establishes a robust data foundation but also guides future research directions. Given its potential as a significant cancer biomarker and therapeutic target, further investigation into LINC00941's differential expression and regulatory mechanisms is essential.

The dysregulation of non-coding RNAs (ncRNAs), specifically microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), leads to the development and advancement of multiple myeloma (MM). miRNAs, in particular, are paramount in post-transcriptional gene regulation, promoting mRNA degradation and translational inhibition. As a result, miRNAs can serve as oncogenes or tumor suppressors depending on the target genes. In MM, miRNA disruption could result in abnormal gene expression responsible for cell growth, apoptosis, and other biological processes pertinent to cancer development. The dysregulated miRNAs inhibit the activity of tumor suppressor genes, contributing to disease progression. Nonetheless, several miRNAs are downregulated in MM and have been identified as gene regulators implicated in extracellular matrix remodeling and cell adhesion. miRNA depletion potentially facilitates the tumor advancement and resistance of therapeutic drugs. Additionally, lncRNAs are key regulators of numerous cellular processes, such as gene expression, chromatin remodeling, protein trafficking, and recently linked MM development. The lncRNAs are uniquely expressed and influence gene expression that supports MM growth, in addition to facilitating cellular proliferation and viability via multiple molecular pathways. miRNA and lncRNA alterations potentially result in anomalous gene expression and interfere with the regular functioning of MM. Thus, this review aims to highlight the dysregulation of these ncRNAs, which engender novel therapeutic modalities for the treatment of MM.

The unnotified or undifferentiable early stages of oral squamous cell carcinoma (OSCC) progression are the prime reasons for late-stage detection and poor survival outcomes of oral cancer. This review summarizes the prior research and recent advancements on the influence of dysregulated non-coding RNA (ncRNA) on cell cycle and their employability as diagnostic and prognostic biomarkers of oral cancer. The literature search was performed using the following keywords: 'serum/saliva non-coding RNAs' and 'serum/saliva non-coding RNAs and cell cycle', 'serum/saliva dysregulated ncRNAs and cell cycle', 'Cdk/CKI and ncRNAs', 'tissue ncRNAs' concerning 'oral cancer''. The compiled data focuses mainly on the diagnostic and prognostic significance of MicroRNAs (miRNAs), Circular RNAs (circRNAs), and Long noncoding RNAs (lncRNAs) on oral cancer and all other cancers as well as subject-relevant articles published in languages other than English are beyond the scope of this review and excluded from the study. Moreover, articles focusing on DNA, protein, and metabolite markers are eliminated from the study. While there exist various potential biomolecules such as DNA, RNA, proteins, metabolites, and specific antigens representing predictive biomarkers in body fluids for oral cancer, this review completely focuses on non-coding RNAs restricted to saliva and blood, picking out a few of the reliable ones amongst the recent investigations based on the sophisticated techniques, cohort, and sensitivity as well as specificity, i.e., salivary miR-1307-5p, miR-3928, hsa_circ_0001874 and ENST00000412740, NR_131012, ENST00000588803, NR_038323, miR-21 in circulation. Thus, further studies are required to clinically confirm the usage of these non-invasive biomarkers in oral cancer.

The natural phenolic compound ellagic acid exerts anti-cancer effects, including activity against colorectal cancer (CRC). Previously, we reported that ellagic acid can inhibit the proliferation of CRC, and can induce cell cycle arrest and apoptosis. This study investigated ellagic acid-mediated anticancer effects using the human colon cancer HCT-116 cell line. After 72 h of ellagic acid treatment, a total of 206 long noncoding RNAs (lncRNAs) with differential expression greater than 1.5-fold were identified (115 down-regulated and 91 up-regulated). Furthermore, the co-expression network analysis of differentially expressed lncRNA and mRNA showed that differential expressed lncRNA might be the target of ellagic acid activity in inhibiting CRC.

Male infertility is a global health issue, affecting over 20 million men worldwide. Genetic factors are crucial in various male infertility forms, including teratozoospermia. Nonetheless, the genetic causes of male infertility remain largely unexplored. In this study, we employed whole-genome sequencing and RNA expression analysis to detect differentially expressed (DE) long-noncoding RNAs (lncRNAs) in teratozoospermia, along with mutations that are exclusive to teratozoospermic individuals within these DE lncRNAs regions. Bioinformatic tools were used to assess variants' impact on lncRNA structure, function, and lncRNA-miRNA interactions. Our analysis identified 1166 unique mutations in teratozoospermic men within DE lncRNAs, distinguishing them from normozoospermic men. Among these, 64 variants in 23 lncRNAs showed potential regulatory roles, 7 variants affected 4 lncRNA structures, while 37 variants in 17 lncRNAs caused miRNA target loss or gain. Pathway Enrichment and Gene Ontology analyses of the genes targeted by the affected miRNAs revealed dysregulated pathways in teratozoospermia and a link between male infertility and cancer. This study lists novel variants and lncRNAs associated for the first time with teratozoospermia. These findings pave the way for future studies aiming to enhance diagnosis and therapy in the field of male infertility.

Gynecologic cancers are a worldwide problem among women. Recently, molecular targeted therapy opened up an avenue for cancer diagnosis and treatment. Long non-coding RNAs (lncRNAs) are RNA molecules (> 200 nt) that are not translated into protein, and interact with DNA, RNA, and proteins. LncRNAs were found to play pivotal roles in cancer tumorigenesis and progression. Nuclear paraspeckle assembly transcript 1 (NEAT1) is a lncRNA that mediates cell proliferation, migration, and EMT in gynecologic cancers by targeting several miRNAs/mRNA axes. Therefore, NEAT1 may function as a potent biomarker for the prediction and treatment of breast, ovarian, cervical, and endometrial cancers. In this narrative review, we summarized various NEAT1-related signaling pathways that are critical in gynecologic cancers. Long non-coding RNA (lncRNA) by targeting various signaling pathways involved in its target genes can regulate the occurrence of gynecologic cancers.

Breast cancer is a leading cause of incidence and mortality in women globally. Identifying new molecular markers can aid in cancer diagnosis, targeted therapy, and treatment monitoring. This study aimed to measure the expression of the X-box binding protein 1 (XBP1) gene, an index of the unfolded protein response (UPR), and long noncoding RNAs (lncRNAs), including Nuclear Enriched Abundant Transcript 1 (NEAT1), Cancer Susceptibility Candidate 2 (CASC2), and Long Intergenic Nonprotein Coding RNA 299 (LINC00299), as possible regulators of the UPR pathway.

Total RNA was extracted from 40 samples of breast tumor tissues and their respective controls. The expression level of lncRNAs CASC2, NEAT1, and LINC00299 was quantified using reverse transcription-polymerase chain reaction (RT-PCR). The ratio of the spliced form of XBP1 to its unspliced form (XBP1u) was determined by PCR and electrophoresis.

The results showed a 2.8-fold increase in the ratio of XBP1s/u in breast cancer tissues compared to adjacent nonmalignant samples (p < 0.05). Additionally, the level of lncRNAs NEAT1, CASC2, and LINC00299 in breast tumor tissues increased significantly by twofold, 1.5-fold, and 2.3-fold, respectively, compared to adjacent nonmalignant samples (p < 0.05).

Based on the association between the expression of lncRNAs CASC2, LINC00299, and NEAT1 and the XBP1s/u ratio, these lncRNAs could be potential regulators of the UPR pathway. Also, CASC2 and NEAT1 genes could be suggested as suitable biomarkers to distinguish cancerous tissue from noncancerous breast tissue due to their significant increase in expression in cancerous samples compared to adjacent noncancerous.

Long non-coding RNA (LncRNA) telomerase RNA component (TERC) has telomerase-dependent and independent activity in numerous cancer types. The present study purposes to demonstrate the role of lncRNA TERC as a diagnostic serum biomarker in colorectal cancer (CRC) patients and the molecular mechanism of lncRNA TERC in inducing tumor in CRC cell lines.

PCR array was performed to examine lncRNAs dysregulated in CRC. LncRNA TERC expression level was evaluated in 70 CRC patients and 35 control subjects using RT-qPCR. Then transfection was performed to build down-expression models of lncRNA TERC. ROC curve analysis was applied to assess the diagnostic value of serum LncRNA CRC. In addition, RT-qPCR was used to detect expression level of lncRNA TERC and β-catenin mRNA. Moreover, ELISA and Western blot were used to detect the level of β-catenin protein in sera of CRC patients and cell lines. The biological functions such as cell growth and migration of CRC cells were assessed using a wound healing assay. Cell cycle analysis and apoptosis analysis were performed using flow cytometry.

The lncRNA TERC is overexpressed in the sera of CRC patients with high diagnostic and stage discrimination accuracy. Furthermore, lncRNA TERC expression was upregulated in CRC cell lines and lncRNA TERC silencing induced cell arrest and apoptosis and inhibited cell migration. Furthermore, inhibition of lncRNA TERC reduces β-catenin protein levels.

The lncRNA TERC could be considered as an early stages CRC diagnostic biomarker with a good ability to discriminate between CRC stages. lncRNA TERC induces CRC by promoting cell migration and evading apoptosis by elevating the level of β-catenin protein.

Notch1 signalling plays a multifaceted role in tissue development and homeostasis. Currently, due to the pivotal role of Notch1 signalling, the relationship between NOTCH1 expression and the development of health disorders is being intensively studied. Nevertheless, Notch1 signalling is not only controlled at the transcriptional level but also by a variety of post-translational events. First is the ligand-dependent mechanical activation of NOTCH receptors and then the intracellular crosstalk with other signalling molecules-among those are long non-coding RNAs (lncRNAs). In this review, we provide a detailed overview of the specific role of lncRNAs in the modulation of Notch1 signalling, from expression to activity, and their connection with the development of health disorders, especially cancers.

Despite the recent advances in cancer therapy, triple-negative breast cancers (TNBCs) are the most relapsing cancer sub-type. It is partly due to their propensity to develop resistance against the available therapies. An intricate network of regulatory molecules in cellular mechanisms leads to the development of resistance in tumors. Non-coding RNAs (ncRNAs) have gained widespread attention as critical regulators of cancer hallmarks. Existing research suggests that aberrant expression of ncRNAs modulates the oncogenic or tumor suppressive signaling. This can mitigate the responsiveness of efficacious anti-tumor interventions. This review presents a systematic overview of biogenesis and down streaming molecular mechanism of the subgroups of ncRNAs. Furthermore, it explains ncRNA-based strategies and challenges to target the chemo-, radio-, and immunoresistance in TNBCs from a clinical standpoint.

Previous studies have shown that the differential expression of lncRNA NR2F1-AS1 is closely related to the prognosis of cancer, but the conclusion is still controversial. Therefore, we conducted a meta-analysis and bioinformatics analysis to explore the correlation between LncRNA NR2F1-AS1 and cancer prognosis.

From the beginning to January 25, 2023, we searched for correlational studies on PubMed, Embase, the Cochrane Library, and Web of Science. We used pooled hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (CIs) to determine the importance of LncRNA NR2F1-AS1 for survival and clinicopathological features of human cancers.

The meta-analysis of 637 patients in the 11 included articles showed that upregulation of LncRNA NR2F1-AS1 was associated with shorter overall survival (HR = 1.46,95%Cl 1.06-2.01, p = 0.02) in cancer patients. In addition, overexpression of LncRNA NR2F1-AS1 predicted TNM tumor stage (OR = 3.37, 95%Cl 2.07-5.48, p < 0.00001), and Distant metastasis (OR = 0.18, 95%Cl 0.06-0.48, p = 0.0007). However, the difference in age (OR = 1.10,95%Cl 0.71-1.71, p = 0.67), gender (OR = 1.26,95%Cl 0.79-2.00, p = 0.34), Lymph node metastasis (OR = 1.44,95%Cl 0.27-7.80, p = 0.67) or larger tumor size (OR = 1.56,95%Cl 0.48-5.08, p = 0.46) was not statistically significant.

Upregulation of LncRNA NR2F1-AS1 was associated with poor prognosis and advanced clinicopathologic features of tumor patients.

Myocardial hypoxia is an important factor causing myocardial infarction (MI). Interestingly, many unknown factors in the molecular mechanism of MI remain unclear. Our study explored the role of lncRNA growth arrest-specific 5 (GAS5) in cell injury under hypoxia.

AS5 expression was assessed in MI and human cardiomyocytes under hypoxia through RT-qPCR assay. Methyl thiazolyl tetrazolium assay, flow cytometry assay, and transwell assay was carried out for cell viability, cell apoptosis, cell migration, and invasion, respectively. The regulatory target of GAS5 was explored through a dual-luciferase reporter assay.

Our findings indicated that the upregulation of GAS5 was related to hypoxia. Downregulation of GAS5 expression could decrease hypoxia-induced cell apoptosis and increase cell migration and invasion. Moreover, GAS 5 targeted miR-21, which regulated the phosphatase and tension homology deleted on chromosome ten gene (PTEN) expression. Furthermore, the knockdown of miR-21 eliminated the effect of GAS5 silencing on cell injury.

These results indicated that lncRNA GAS5 silencing decreased cardiomyocyte injury by hypoxia-induced through regulating miR-21/PTEN.

Breast cancer is the most frequently diagnosed malignancy and the leading cause of cancer-related death in women worldwide. Breast cancer development and progression are mainly associated with tumor-intrinsic alterations in diverse genes and signaling pathways and with tumor-extrinsic dysregulations linked to the tumor immune microenvironment. Significantly, abnormal expression of lncRNAs affects the tumor immune microenvironment characteristics and modulates the behavior of different cancer types, including breast cancer. In this review, we provide the current advances about the role of lncRNAs as tumor-intrinsic and tumor-extrinsic modulators of the antitumoral immune response and the immune microenvironment in breast cancer, as well as lncRNAs which are potential biomarkers of tumor immune microenvironment and clinicopathological characteristics in patients, suggesting that lncRNAs are potential targets for immunotherapy in breast cancer.

Background: Breast cancer (BRCA) represents the most frequent diagnosed malignancy in women worldwide. Despite treatment advances, BRCAs eventually develop resistance to targeted therapies, resulting in poor prognosis. The identification of new biomarkers, like immune-related long non-coding RNAs (lncRNAs), could contribute to the clinical management of BRCA patients. In this report, we evaluated the LINC00426 expression in PAM50 BRCA subtypes from two clinical independent cohorts (BRCA-TCGA and GEO-GSE96058 datasets). Methods and results: Using Cox regression models and Kaplan-Meier survival analyses, we identified that LINC00426 expression was a consistent overall survival (OS) predictor in luminal B (LB) BRCA patients. Subsequently, differential gene expression and gene set enrichment analyses identified that LINC00426 expression was associated with different immune-related and cancer-related pathways and processes in LB BRCA. Additionally, the LINC00426 expression was correlated with the infiltration level of diverse immune cell populations, alongside immune checkpoint and cytolytic activity-related gene expression. Conclusion: This evidence suggests that LINC00426 is a potential biomarker of immune phenotype and an OS predictor in PAM50 LB BRCA.

Bladder cancer (BC) is the tenth most common cancer, with urothelial carcinoma representing about 90% of all BC, including neoplasms and carcinomas of different grades of malignancy. Urinary cytology has a significant role in BC screening and surveillance, although it has a low detection rate and high dependence on the pathologist's experience. The currently available biomarkers are not implemented into routine clinical practice due to high costs or low sensitivity. In recent years, the role of lncRNAs in BC has emerged, even though it is still poorly explored. We have previously shown that the lncRNAs Metallophosphoesterase Domain-Containing 2 Antisense RNA 1 (MPPED2-AS1), Rhabdomyosarcoma-2 Associated Transcript (RMST), Kelch-like protein 14 antisense (Klhl14AS) and Prader Willi/Angelman region RNA 5 (PAR5) are involved in the progression of different types of cancers. Here, we investigated the expression of these molecules in BC, first by interrogating the GEPIA database and observing a different distribution of expression levels between normal and cancer specimens. We then measured them in a cohort of neoplastic bladder lesions, either benign or malignant, from patients with suspicion of BC undergoing transurethral resection of bladder tumor (TURBT). The total RNA from biopsies was analyzed using qRT-PCR for the expression of the four lncRNA genes, showing differential expression of the investigated lncRNAs between normal tissue, benign lesions and cancers. In conclusion, the data reported here highlight the involvement of novel lncRNAs in BC development, whose altered expression could potentially affect the regulatory circuits in which these molecules are involved. Our study paves the way for testing lncRNA genes as markers for BC diagnosis and/or follow-up.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection which is commonly known as COVID-19 (COronaVIrus Disease 2019) has creeped into the human population taking tolls of life and causing tremendous economic crisis. It is indeed crucial to gain knowledge about their characteristics and interactions with human host cells. It has been shown that the majority of our genome consists of non-coding RNAs. Non-coding RNAs including micro RNAs (miRNAs) and long non-coding RNAs (lncRNAs) display significant roles in regulating gene expression in almost all cancers and viral diseases. It is intriguing that miRNAs and lncRNAs remarkably regulate the function and expression of major immune components of SARS-CoV-2. MiRNAs act via RNA interference mechanism in which they bind to the complementary sequences of the viral RNA strand, inducing the formation of silencing complex that eventually degrades or inhibits the viral RNA and viral protein expression. LncRNAs have been extensively shown to regulate gene expression in cytokine storm and thus emerges as a critical target for COVID-19 treatment. These lncRNAs also act as competing endogenous RNAs (ceRNAs) by sponging miRNAs and thus affecting the expression of downstream targets during SARS-CoV-2 infection. In this review, we extensively discuss the role of miRNAs and lncRNAs, describe their mechanism of action and their different interacting human targets cells during SARS-CoV-2 infection. Finally, we discuss possible ways how an interference with their molecular function could be exploited for new therapies against SARS-CoV-2.

Prostate cancer (PCa) is as a serious threat to male's health around the world. Recent studies have indicated that long non-coding RNAs (lncRNAs) occupy an important position in various human cancers. However, the function and mechanism of lncRNA DNMBP antisense RNA 1 (DNMBP-AS1) in PCa is rarely investigated. RT-qPCR analysis was used to test gene expression. CCK-8, colony formation, EdU staining and transwell assays were conducted to assess the function of DNMBP-AS1 on PCa cell behaviors. RNA pull down, RIP and luciferase reporter assays were implemented to verify the mechanism of DNMBP-AS1. DNMBP-AS1 was obviously up-regulated in PCa cell lines. Functionally, DNMBP-AS1 knockdown weakened cell proliferation, migration and invasion of PCa. Mechanistically, DNMBP-AS1 sponged microRNA-6766-3p (miR-6766-3p) to regulate lysocardiolipin acyltransferase 1 (LCLAT1) expression. Furthermore, DNMBP-AS1 could stabilize LCLAT1 expression by recruiting ELAV like RNA binding protein 1 (ELAVL1). Consequently, rescue assays demonstrated that DNMBP-AS1 regulated PCa cell proliferation, migration and invasion through enhancing LCLAT1 expression. Collectively, we elucidated the function and regulatory mechanism of DNMBP-AS1 and provided the first evidence of DNMBP-AS1 as a driver for PCa.

Cells maintain homeostasis in response to environmental stress through specific cell stress responses. Hypoxic stress, well known to be associated with diverse solid tumors, is one of the main reasons for cancer-related mortality. Although cells can balance themselves well during hypoxic stress, the underlying molecular mechanisms are not well understood. The enhanced appreciation of diverse roles played by noncoding transcriptome and epigenome in recent years has brought to light the involvement of noncoding RNAs and epigenetic modifiers in hypoxic regulation. The emergence of techniques like deep sequencing has facilitated the identification of large numbers of long noncoding RNAs (lncRNAs) that are differentially regulated in various cancers. Similarly, proteomic studies have identified diverse epigenetic modifiers such as HATs, HDACs, DNMTs, polycomb groups of proteins, and their possible roles in the regulation of hypoxia. The crosstalk between lncRNAs and epigenetic modifiers play a pivotal role in hypoxia-induced cancer initiation and progression. Besides the lncRNAs, several other noncoding RNAs like circular RNAs, miRNAs, and so forth are also expressed during hypoxic conditions. Hypoxia has a profound effect on the expression of noncoding RNAs and epigenetic modifiers. Conversely, noncoding RNAs/epigenetic modifies can regulate the hypoxia signaling axis by modulating the stability of the hypoxia-inducible factors (HIFs). The focus of this review is to illustrate the molecular orchestration underlying hypoxia biology, especially in cancers, which can help in identifying promising therapeutic targets in hypoxia-induced cancers. This article is categorized under: RNA Turnover and Surveillance > Regulation of RNA Stability RNA in Disease and Development > RNA in Disease RNA Structure and Dynamics > RNA Structure, Dynamics and Chemistry.

Alphaviruses are important human and animal pathogens that can cause a range of debilitating symptoms and are found worldwide. These include arthralgic diseases caused by Old-World viruses and encephalitis induced by infection with New-World alphaviruses. Non-coding RNAs do not encode for proteins, but can modulate cellular response pathways in a myriad of ways. There are several classes of non-coding RNAs, some more well-studied than others. Much research has focused on the mRNA response to infection against alphaviruses, but analysis of non-coding RNA responses has been more limited until recently. This review covers what is known regarding host cell non-coding RNA responses in alphavirus infections and highlights gaps in the knowledge that future research should address.

Ovarian cancer (OC) is one of the most common causes of cancer-related death in women worldwide. Its five-year survival rates are worse than the two most common gynecological cancers, cervical and endometrial. This is because it is asymptomatic in the early stages and usually detected in the advanced metastasized stage. Thus, survival is increasingly dependent on timely diagnosis. The delay in detection is contributed partly by the occurrence of non-specific clinical symptoms in the early stages and the lack of effective biomarkers and detection approaches. This underlines the need for biomarker identification and clinical validation, enabling earlier diagnosis, effective prognosis, and response to therapy. Apart from the traditional diagnostic biomarkers for OC, several new biomarkers have been delineated using advanced high-throughput molecular approaches in recent years. They are currently being clinically evaluated for their true diagnostic potential. In this chapter, we document the commonly utilized traditional screening markers and recently identified emerging biomarkers in OC diagnosis, focusing on secretory and protein biomarkers. We also briefly reviewed the recent advances and prospects in OC diagnosis.

Cervical cancer is a significant public health problem in developing countries, as most cases present at an advanced stage. This review aimed to analyze the role of noncoding RNAs as diagnostic and prognostic biomarkers in cervical cancers. Published studies on specific microRNA signatures in body fluids and cervical cancer tissues are highly heterogeneous, and there are no validated assays. The precision of the various immune-associated long noncoding (lncRNA) signatures should be assessed in clinical samples. Even though lncRNAs are tissue and cancer-specific, safe and appropriate methods for delivery to tumor tissues, toxicities and side effects are to be explored. Few studies have evaluated deregulated lncRNA expression levels with clinicopathological factors in a limited number of clinical samples. Prospective studies assessing the diagnostic and prognostic roles of circulating lncRNAs and P-Element-induced wimpy testis interacting PIWI RNAs (Piwil RNAs) in cervical cancer cases are essential. For the clinical application of lnc-RNA-based biomarkers, comprehensive research is needed as the impact of noncoding transcripts on molecular pathways is complex. The standardization and validation of deregulated ncRNAs in noninvasive samples of cervical cancer cases are needed.

Age-related macular degeneration (AMD) is an ever-increasing, insidious disease which reduces the quality of life of millions of elderly people around the world. AMD is characterised by damage to the retinal pigment epithelium (RPE) in the macula region of the retina. The origins of this multi-factorial disease are complex and still not fully understood. Oxidative stress and mitochondrial imbalance in the RPE are believed to be important factors in the development of AMD. In this review, the regulation of the mitochondrial function and antioxidant stress response by non-coding RNAs (ncRNAs), newly emerged epigenetic factors, is discussed. These molecules include microRNAs, long non-coding RNAs, and circular non-coding RNAs. They act mainly as mRNA suppressors, controllers of other ncRNAs, or by interacting with proteins. We include here examples of these RNA molecules which affect various mitochondrial processes and antioxidant signaling of the cell. As a future prospect, the possibility to manipulate these ncRNAs to strengthen mitochondrial and antioxidant response functions is discussed. Non-coding RNAs could be used as potential diagnostic markers for AMD, and in the future, also as therapeutic targets, either by suppressing or increasing their expression. In addition to AMD, it is possible that non-coding RNAs could be regulators in other oxidative stress-related degenerative diseases.

Cardiovascular disorders such as heart failure are leading causes of mortality. Patient stratification via identification of novel biomarkers could improve management of cardiovascular diseases of complex etiologies. Long-noncoding RNAs (lncRNAs) are highly tissue-specific in nature and have emerged as important biomarkers in human diseases. In this study, we aimed to identify cardiac-enriched lncRNAs as potential biomarkers for cardiovascular conditions. Deep RNA sequencing and quantitative PCR identified differentially expressed lncRNAs between failing and non-failing hearts. An independent dataset was used to evaluate the enrichment of lncRNAs in normal hearts. We identified a panel of 2906 lncRNAs, named FIMICS, that were either cardiac-enriched or differentially expressed between failing and non-failing hearts. Expression of lncRNAs in blood samples differentiated patients with myocarditis and acute myocardial infarction. We hereby present the FIMICS panel, a readily available tool to provide insights into cardiovascular pathologies and which could be helpful for diagnosis, monitoring and prognosis purposes.

Acute lung injury (ALI) and its severe form, acute respiratory distress syndrome (ARDS), represent an acute stage of lung inflammation where the alveolar epithelium loses its functionality. ALI has a devastating impact on the population as it not only has a high rate of incidence, but also has high rates of morbidity and mortality. Due to the involvement of multiple factors, the pathogenesis of ALI is complex and is not fully understood yet. Long noncoding RNAs (lncRNAs) are a group of non-protein-coding transcripts longer than 200 nucleotides. Growing evidence has shown that lncRNAs have a decisive role in the pathogenesis of ALI. LncRNAs can either promote or hinder the development of ALI in various cell types in the lungs. Mechanistically, current studies have found that lncRNAs play crucial roles in the pathogenesis of ALI via the regulation of small RNAs (e.g., microRNAs) or downstream proteins. Undoubtedly, lncRNAs not only have the potential to reveal the underlying mechanisms of ALI pathogenesis but also serve as diagnostic and therapeutic targets for the therapy of ALI.

Lately, the interest in long non-coding RNAs (lncRNAs) as potential drug targets and predictive markers in the context of HIV-1 has peaked, but their in vivo expression and regulation remains largely unexplored. Therefore, the present study examined lncRNA expression patterns during a clinical antiretroviral treatment interruption (ATI) trial. Peripheral blood mononuclear cells were isolated from ten patients at four timepoints: prior to ATI, 7-15 days after stop, at viral rebound and 3 months post antiretroviral therapy re-initiation. RNA was extracted and RT-qPCR on five known HIV-1-related lncRNAs (HEAL, MALAT1, NEAT1, GAS5 and NRON) was performed and correlated with HIV-1 and host marker expression. All lncRNAs correlated stronger with interferon stimulated genes (ISGs) than with HIV-1 reservoir and replication markers. However, one lncRNA, HEAL, showed significant upregulation at viral rebound during ATI compared to baseline and re-initiation of therapy (p = 0.0010 and p = 0.0094, respectively), following a similar viral-load-driven expression pattern to ISGs. In vitro knockdown of HEAL caused a significant reduction in HIV-1 infection levels, validating HEAL's importance for HIV-1 replication. We conclude that the HIV-1-promoting lncRNA HEAL is upregulated at viral rebound during ATI, most likely induced by viral cues.

Cancer consists of a group of diseases with the salient properties of an uncontrolled cell cycle, metastasis, and evasion of the immune response, mainly driven by the genomic instability of somatic cells and the physicochemical environment. Long noncoding RNAs (lncRNAs) are defined as noncoding RNAs with a length of more than 200 nucleotides. LncRNA dysregulation participates in diverse disease types and is tightly associated with patient clinical features, such as age, disease stage, and prognosis. In addition, an increasing number of lncRNAs have been confirmed to regulate a series of biological and pathological processes through numerous mechanisms. The lncRNA epidermal growth factor receptor antisense RNA 1 (EGFR-AS1) was recently discovered to be aberrantly expressed in many types of diseases, particularly in cancers. A high level of EGFR-AS1 was demonstrated to correlate with multiple patient clinical characteristics. More importantly, EGFR-AS1 was found to be involved in the mediation of various cellular activities, including cell proliferation, invasion, migration, chemosensitivity, and stemness. Therefore, EGFR-AS1 is a promising marker for cancer management. In this review, we introduce the expression profile, molecular mechanisms, biological functions, and clinical value of EGFR-AS1 in cancers.

Recent reports show that long non-coding RNAs (lncRNAs) have inefficient splicing and fewer alternative splice variants than mRNAs. Here, we have explored the efficiency of lncRNAs and mRNAs in producing various splice variants, given the number of exons in humans and mice. Intriguingly, lncRNAs produce more splice variants per exon, referred to as Transcript Complexity, than mRNAs. Most lncRNA splice variants are the product of the alternative last exon and exon skipping. LncRNAs and mRNAs with higher transcript complexity have shorter intron lengths. Longer exon length and GC/AG at 5'/3' splice sites are associated with higher transcript complexity in lncRNAs. Lastly, our results indicate that inefficient splicing of lncRNAs may facilitate multiple introns splicing and, thus, more spliced products per exon.

LINC00324 is a 2082 bp intergenic noncoding RNA. Aberrant expression of LINC00324 was associated with the risk of 11 tumors and was closely associated with clinicopathological features and prognostic levels of 7 tumors. LINC00324 can sponge multiple miRNAs to form complex ceRNA networks, and can also recruit transcription factors and bind RNA-binding protein HuR, thereby regulating the expression of a number of downstream protein-coding genes. LINC00324 is involved in 4 signaling pathways, including the PI3K/AKT signaling pathway, cell cycle regulatory pathway, Notch signaling pathway, and Jak/STAT3 signaling pathway. High expression of LINC00324 was associated with larger tumors, a higher degree of metastasis, a higher TNM stage and clinical stage, and shorter OS. Currently, four downstream genes in the LINC00324 network have targeted drugs. In this review, we summarize the molecular mechanisms and clinical value of LINC00324 in tumors and discuss future directions and challenges for LINC00324 research.