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Long non‐coding RNAs (lncRNAs) are well known as crucial regulators to breast cancer development and are implicated in controlling autophagy. LncRNAs are also emerging as valuable prognostic factors for breast cancer patients. It is critical to identify autophagy‐related lncRNAs with prognostic value in breast cancer. In this study, we identified autophagy‐related lncRNAs in breast cancer by constructing a co‐expression network of autophagy‐related mRNAs‐lncRNAs from The Cancer Genome Atlas (TCGA). We evaluated the prognostic value of these autophagy‐related lncRNAs by univariate and multivariate Cox proportional hazards analyses and eventually obtained a prognostic risk model consisting of 11 autophagy‐related lncRNAs (U62317.4, LINC01016, LINC02166, C6orf99, LINC00992, BAIAP2‐DT, AC245297.3, AC090912.1, Z68871.1, LINC00578 and LINC01871). The risk model was further validated as a novel independent prognostic factor for breast cancer patients based on the calculated risk score by Kaplan‐Meier analysis, univariate and multivariate Cox regression analyses and time‐dependent receiver operating characteristic (ROC) curve analysis. Moreover, based on the risk model, the low‐risk and high‐risk groups displayed different autophagy and oncogenic statues by principal component analysis (PCA) and Gene Set Enrichment Analysis (GSEA) functional annotation. Taken together, these findings suggested that the risk model of the 11 autophagy‐related lncRNAs has significant prognostic value for breast cancer and might be autophagy‐related therapeutic targets in clinical practice.

Cancer constitutes a significant public health concern, and addressing the challenge of cancer holds paramount importance and requires immediate attention. Epigenetic alterations, encompassing DNA methylation, have emerged as pivotal contributors to the development of diverse cancer types. These modifications exert their influence by modulating chromatin structure, gene expression patterns and other nuclear processes, thereby influencing cancer pathogenesis. Over the last two decades, an increasing body of evidence has established the involvement of DNA methyltransferase 1 (DNMT1) in various aspects of cancer development, including tumorigenesis, aggressiveness and treatment response. Furthermore, non‐coding RNAs (ncRNAs), such as microRNAs (miRNAs) and long non‐coding RNAs (lncRNAs), are increasingly recognised as significant modulators in diverse biological processes, encompassing metastasis, apoptosis, cell proliferation and differentiation. Several recent studies have elucidated the intricate relationship between epigenetic machinery, specifically DNMT1, and the expression of ncRNAs in the context of cancer. In this review, we provide a comprehensive overview of the interaction between DNMT1 and ncRNAs in cancer pathogenesis. Furthermore, we discuss the important role of the ncRNAs‐DNMT1 axis in cancer stem cells and cancer therapy resistance as critical issues in cancer therapy. Finally, we demonstrate that herbal medicine and synthetic RNA molecules regulate DNMT1 activity and hold great promise in cancer treatment.

Early-stage detection of leukemia is a critical determinant for successful treatment of the disease and can increase the survival rate of leukemia patients. The factors limiting the current screening approaches to leukemia include low sensitivity and specificity, high costs, and a low participation rate. An approach based on novel and innovative biomarkers with high accuracy from peripheral blood offers a comfortable and appealing alternative to patients, potentially leading to a higher participation rate.Recently, non-coding RNAs due to their involvement in vital oncogenic processes such as differentiation, proliferation, migration, angiogenesis and apoptosis have attracted much attention as potential diagnostic and prognostic biomarkers in leukemia. Emerging lines of evidence have shown that the mutational spectrum and dysregulated expression of non-coding RNA genes are closely associated with the development and progression of various cancers, including leukemia. In this review, we highlight the expression and functional roles of different types of non-coding RNAs in leukemia and discuss their potential clinical applications as diagnostic or prognostic biomarkers and therapeutic targets.

Background N6-methyladenosine (m6A) is the most prevalent RNA epigenetic regulation in eukaryotic cells. However, understanding of m6A in colorectal cancer (CRC) is very limited. We designed this study to investigate the role of m6A in CRC. Methods Expression level of METTL14 was extracted from public database and tissue array to investigate the clinical relevance of METTL14 in CRC. Next, gain/loss of function experiment was used to define the role of METTL14 in the progression of CRC. Moreover, transcriptomic sequencing (RNA-seq) was applied to screen the potential targets of METTL14. The specific binding between METTL14 and presumed target was verified by RNA pull-down and RNA immunoprecipitation (RIP) assay. Furthermore, rescue experiment and methylated RNA immunoprecipitation (Me-RIP) were performed to uncover the mechanism. Results Clinically, loss of METTL14 correlated with unfavorable prognosis of CRC patients. Functionally, knockdown of METTL14 drastically enhanced proliferative and invasive ability of CRC cells in vitro and promoted tumorigenicity and metastasis in vivo. Mechanically, RNA-seq and Me-RIP identified lncRNA XIST as the downstream target of METTL14. Knockdown of METTL14 substantially abolished m6A level of XIST and augmented XIST expression. Moreover, we found that m6A-methylated XIST was recognized by YTHDF2, a m6A reader protein, to mediate the degradation of XIST . Consistently, XIST expression negatively correlated with METTL14 and YTHDF2 in CRC tissues. Conclusion Our findings highlight the function and prognostic value of METTL14 in CRC and extend the understanding of the importance of RNA epigenetics in cancer biology.

Chemoresistance, whether intrinsic or acquired, is a major obstacle in the treatment of cancer. The resistance of cancer cells to chemotherapeutic drugs can result from various mechanisms. Over the last decade, it has been reported that 1ong noncoding RNAs (lncRNAs) can mediate carcinogenesis and drug resistance/sensitivity in cancer cells. This article reviews, in detail, recent studies regarding the roles of lncRNAs in mediating drug resistance.

Oral squamous cell carcinoma (OSCC), the eighth most prevalent cancer in the world, arises from the interaction of multiple factors including tobacco, alcohol consumption, and betel quid. Chemotherapeutic agents such as cisplatin, 5‐fluorouracil, and paclitaxel have now become the first‐line options for OSCC patients. Nevertheless, most OSCC patients eventually acquire drug resistance, leading to poor prognosis. With the discovery and identification of non‐coding RNAs (ncRNAs), the functions of dysregulated ncRNAs in OSCC development and drug resistance are gradually being widely recognized. The mechanisms of drug resistance of OSCC are intricate and involve drug efflux, epithelial‐mesenchymal transition, DNA damage repair, and autophagy. At present, strategies to explore the reversal of drug resistance of OSCC need to be urgently developed. Nano‐delivery and self‐cellular drug delivery platforms are considered as effective strategies to overcome drug resistance due to their tumor targeting, controlled release, and consistent pharmacokinetic profiles. In particular, the combined application of new technologies (including CRISPR systems) opened up new horizons for the treatment of drug resistance of OSCC. Hence, this review explored emerging regulatory functions of ncRNAs in drug resistance of OSCC, elucidated multiple ncRNA‐meditated mechanisms of drug resistance of OSCC, and discussed the potential value of drug delivery platforms using nanoparticles and self‐cells as carriers in drug resistance of OSCC. The mechanisms of drug resistance are intricate and involve drug efflux, epithelial mesenchymal transition, DNA damage repair, and autophagy. Nano‐delivery and self‐cellular drug delivery platforms have a broad prospective for alleviating OSCC drug resistance. In particular, the combined application of new technologies (including CRISPR systems) opens up new horizons for treatment of OSCC drug resistance.

Non-coding RNAs are a diverse group of RNAs that are generally not translated into proteins, and control gene expression and other cellular processes through a myriad of mechanisms. Non-coding RNAs are fragmented to regulate cellular processes such as ribosomal RNA maturation, reverse transcription and degradation of nascent transcripts, among other functions. Non-coding RNAs and their fragments interact with Toll-like receptors (TLRs) to induce the activation of the innate and adaptative immune system, which are important for counteracting viral and bacterial infections as well as for triggering ischemia-related cytotoxic effects in the brain. As the study of these interactions progresses, novel functions are being elucidated, such as their participation in viral reactivation in the brain. Due to their importance as pattern recognition receptor families, TLRs may be potential therapeutic targets for the treatment of autoimmune diseases, viral diseases and cancer. TLR activators are currently used for the treatment of different types of cancer and several other biomolecules are still under investigation to progress towards clinical use. The ncRNAs and their fragments also function as ligands for TLRs, but further study of non-coding RNAs and their action on TLRs will allow the elucidation of new TLR agonists and antagonists to establish successful immunotherapies. The aim of the present review is to show the existing evidence on TLR activation by ncRNAs and their fragments, with special emphasis on the diseases in which they are involved and on the potential of the study of these interactions for the identification of therapeutic targets and development of therapies.

The term autophagy describes a process that supports nutrient cycling and metabolic adaptation that is accomplished via multistep lysosomal degradation. These activities modulate cell, tissue and internal environment stability, and can also affect the occurrence and development of cancer. Previous studies have mostly described autophagy as having dual effects in cancer, serving to limit tumorigenesis in the early stages of cancer, but promoting tumor progression in certain types of cancer. There have been indications in recent years that microRNAs (miRNAs/miRs) and long non-coding RNAs (lncRNAs), as types of non-coding RNAs, play major roles in the occurrence, invasion, development and drug resistance of hepatocellular carcinoma (HCC) and in the migration of HCC cells by governing HCC cell autophagy. Therefore, understanding which miRNAs and lncRNAs play such roles and the relevant molecular mechanisms is critical. The present review highlights the significant functions of miRNAs and lncRNAs in the regulation of autophagy in HCC and the relevant mechanisms, aiming to provide novel insight into HCC therapeutics.

Lung cancer remains a significant global health challenge, largely due to difficulties in early detection and the lack of effective therapeutic strategies for more advanced-stage disease. Elucidating the molecular mechanisms underlying lung carcinogenesis and identifying reliable biomarkers is of urgent importance. Long non-coding RNAs (lncRNAs), a class of transcripts of >200 nucleotides without protein-coding potential, have recently emerged as key regulators of tumor cell invasion, metastasis, proliferation, apoptosis and angiogenesis. Accumulating evidence suggests that lncRNAs hold notable promise as diagnostic and prognostic biomarkers in lung cancer. However, a comprehensive overview that integrates their mechanistic roles, clinical potential and the technological advances in their detection, while critically addressing the associated challenges, is lacking, to the best of the authors' knowledge. In the present review, a summary of recent advances in the mechanistic roles of lncRNAs during lung cancer progression and their involvement in therapy response and chemoresistance was provided, along with an up-to-date discussion of emerging detection technologies and their implications for clinical translation. The advantages, limitations and challenges of using lncRNAs as diagnostic or prognostic biomarkers in lung cancer are discussed. By synthesizing these aspects, the present review aimed to highlight the novel insights into lncRNAs and outline future research directions, thereby addressing a critical gap in the current literature.

Highly up‐regulated in liver cancer (HULC) was originally identified as the most overexpressed long non‐coding RNA in hepatocellular carcinoma. Since its discovery, the aberrant up‐regulation of HULC has been demonstrated in other cancer types, including gastric cancer, pancreatic cancer, osteosarcoma and hepatic metastasis of colorectal cancer. Recent discoveries have also shed new light on the upstream molecular mechanisms underlying HULC deregulation. As an oncogene, HULC promotes tumorigenesis by regulating multiple pathways, such as down‐regulation of EEF1E1, promotion of abnormal lipid metabolism, and up‐regulation of sphingosine kinase 1. Pertinent to clinical practice, a genetic variant in the HULC gene has been found to alter the risk for hepatocellular carcinoma and oesophageal cancer, whereas cancer patients with high or low expression of HULC exhibit different clinical outcome. These findings highlighted the pathogenic role and clinical utility of HULC in human cancers. Further efforts are warranted to promote the development of HULC‐directed therapeutics.