Non-coding RNA Research最新文献

{"title":"Identification and validation of lncRNA mutation hotspot SNPs associated with myasthenia gravis susceptibility","authors":"Ni He ,&nbsp;Liting Tian ,&nbsp;Jingnan Jin ,&nbsp;Yue Liu ,&nbsp;Lifang Li ,&nbsp;Xiaokun Wang ,&nbsp;Danyang Li ,&nbsp;Xia Wang ,&nbsp;Xiaoju Li ,&nbsp;Zihong Chen ,&nbsp;Lanxin Zhang ,&nbsp;Lukuan Qiao ,&nbsp;Shangwei Ning ,&nbsp;Lihua Wang ,&nbsp;Jianjian Wang","doi":"10.1016/j.ncrna.2024.12.012","DOIUrl":"10.1016/j.ncrna.2024.12.012","url":null,"abstract":"<div><h3>Background</h3><div>Myasthenia gravis (MG) is an autoimmune disorder caused by antibodies that target the postsynaptic muscle membrane. Recent evidence suggests that genetic variants and long noncoding RNAs (lncRNAs) play crucial roles in the pathogenesis of MG. The purpose of this study was to investigate the associations between lncRNA-related single-nucleotide polymorphisms (SNPs) and MG susceptibility in Chinese populations.</div></div><div><h3>Methods</h3><div>First, we identified lncRNA mutation hotspot regions based on the improved Kolmogorov‒Smirnov test and the cumulative hypergeometric distribution principle. Next, we further identified lncRNA mutation hotspot SNPs by calculating conservative scores. Finally, experiments were conducted to verify the associations between lncRNA mutation hotspot SNPs and MG susceptibility. A total of 82 patients with MG and 82 healthy controls were recruited for genotyping of lncRNA mutation hotspot SNPs using the SNaPshot technique. Quantitative real-time PCR was used to investigate lncRNA expression in 34 patients with MG and 37 healthy controls.</div></div><div><h3>Results</h3><div>In the multistep calculation, 14 candidate SNPs of 3 lncRNAs (AL031686.1, NONHSAT028539.2 and AC245014.3) in MG were identified as mutation hotspot SNPs. The genotyping results of the 14 SNPs in our study revealed no statistically significant differences in the frequencies of genotypes and alleles between patients with MG and controls. However, in the lncRNA AL031686.1, rs1000383 and rs6094353 were in perfect linkage disequilibrium (LD) and were associated with an increased risk of ocular MG. Additionally, rs6094347 was associated with an increased risk of ocular MG. Nevertheless, no SNP was found to be associated with factors such as sex, age, the presence or absence of thymoma, or the genetic model of MG. Further experiments revealed that NONHSAT028539.2 expression was upregulated in peripheral blood mononuclear cells (PBMCs) from patients with MG compared with those from healthy controls.</div></div><div><h3>Conclusion</h3><div>In our study, we did not find an association between the 14 mutation hotspot SNPs of lncRNAs and susceptibility to MG. However, we observed that the rs6094347 and rs1000383/rs6094353 polymorphisms in the lncRNA AL031686.1 were associated with the risk of ocular MG.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 209-219"},"PeriodicalIF":5.9,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786913/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances of miR-23 in human diseases and growth development","authors":"Xu Qian ,&nbsp;Yongwei Jiang ,&nbsp;Yadi Yang ,&nbsp;Yukun Zhang ,&nbsp;Na Xu ,&nbsp;Bin Xu ,&nbsp;Ke Pei ,&nbsp;Zhi Yu ,&nbsp;Wei Wu","doi":"10.1016/j.ncrna.2024.12.010","DOIUrl":"10.1016/j.ncrna.2024.12.010","url":null,"abstract":"<div><div>MicroRNA (miRNA) is broadly manifested in eukaryotes and serves as a critical function in biological development and disease occurrence. With the rapid advancement of experimental research tools, researchers have discovered functional correlations among different miRNA isoforms and clusters within the same miRNA family. As a highly conserved member in the miR-23-27-24 cluster, miR-23 exhibits different isoforms and participates in various essential development. Although the miR-23-27-24 cluster has overlapping target sites, their differential expression can demonstrate independent biological functions. Furthermore, the untapped effects of miR-23 on organisms, whether as a functional cluster or a single regulator, has not been systematically elucidated yet. In this review article, we analyze the genomic location of miR-23 and its sequence variances among its isoforms or family members while summarizing its regulatory functions in metabolic diseases, immune responses, cardiovascular diseases, cancer, organ development as well as nervous system function. This review highlights the significant role of miR-23 as a biomarker for disease diagnosis and a key regulatory factor in pathogenesis, which can help us comprehend the diverse functions of miRNAs and provide a theoretical reference for the functional differences among miRNA isoforms.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 220-233"},"PeriodicalIF":5.9,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of tRNA-Derived small RNAs (tsRNAs) in pancreatic cancer and acute pancreatitis","authors":"Yan Pan ,&nbsp;Xiaowei Ying ,&nbsp;Xueting Zhang ,&nbsp;Hongting Jiang ,&nbsp;Junjie Yan ,&nbsp;Shiwei Duan","doi":"10.1016/j.ncrna.2024.12.011","DOIUrl":"10.1016/j.ncrna.2024.12.011","url":null,"abstract":"<div><div>tRNA-derived small RNAs (tsRNAs), encompassing tRNA fragments (tRFs) and tRNA-derived stress-induced RNAs (tiRNAs), represent a category of non-coding small RNAs (sncRNAs) that are increasingly recognized for their diverse biological functions. These functions include gene silencing, ribosome biogenesis, retrotransposition, and epigenetics. tsRNAs have been identified as key players in the progression of various tumors, yet their specific roles in pancreatic cancer (PC) and acute pancreatitis (AP) remain largely unexplored. Pancreatic cancer, particularly pancreatic ductal adenocarcinoma, is notorious for its high mortality rate and extremely low patient survival rate, primarily due to challenges in early diagnosis. Similarly, acute pancreatitis is a complex and significant disease. This article reviews the roles of 18 tsRNAs in PC and AP, focusing on their mechanisms of action and potential clinical applications in these two diseases. These tsRNAs influence the progression of pancreatic cancer and acute pancreatitis by modulating various pathways, including ZBP1/NLRP3, Hippo, PI3K/AKT, glycolysis/gluconeogenesis, and Wnt signaling. Notably, the dysregulation of tsRNAs is closely linked to critical clinical factors in pancreatic cancer and acute pancreatitis, such as lymph node metastasis, tumor-node-metastasis (TNM) stage, overall survival (OS), and disease-free survival (DFS). This article not only elucidates the mechanisms by which tsRNAs affect pancreatic cancer and acute pancreatitis but also explores their potential as biomarkers and therapeutic targets for pancreatic cancer. The insights provided here offer valuable references for future research, highlighting the importance of tsRNAs in the diagnosis and treatment of these challenging diseases.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 200-208"},"PeriodicalIF":5.9,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of long non-coding RNAs in cardiovascular diseases: A comprehensive review","authors":"Xuena Xie ,&nbsp;Meiwen Huang ,&nbsp;Shudong Ma ,&nbsp;Qiqi Xin ,&nbsp;Yuying Wang ,&nbsp;Lantian Hu ,&nbsp;Han Zhao ,&nbsp;Pengqi Li ,&nbsp;Mei Liu ,&nbsp;Rong Yuan ,&nbsp;Yu Miao ,&nbsp;Yizhun Zhu ,&nbsp;Weihong Cong","doi":"10.1016/j.ncrna.2024.12.009","DOIUrl":"10.1016/j.ncrna.2024.12.009","url":null,"abstract":"<div><div>Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality worldwide, posing significant challenges to healthcare systems. Despite advances in medical interventions, the molecular mechanisms underlying CVDs are not yet fully understood. For decades, protein-coding genes have been the focus of CVD research. However, recent advances in genomics have highlighted the importance of long non-coding RNAs (lncRNAs) in cardiovascular health and disease. Changes in lncRNA expression specific to tissues may result from various internal or external factors, leading to tissue damage, organ dysfunction, and disease. In this review, we provide a comprehensive discussion of the regulatory mechanisms underlying lncRNAs and their roles in the pathogenesis and progression of CVDs, such as coronary heart disease, atherosclerosis, heart failure, arrhythmias, cardiomyopathies, and diabetic cardiomyopathy, to explore their potential as therapeutic targets and diagnostic biomarkers.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 158-187"},"PeriodicalIF":5.9,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11783329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long non-coding RNA AK023617 orchestrates atherosclerosis by regulating the circadian rhythm of immunity-related GTPase family M protein in macrophages","authors":"Rongzhe Lu ,&nbsp;Hengxuan Cai ,&nbsp;Yige Liu ,&nbsp;Guanpeng Ma ,&nbsp;Jiaxin Wang ,&nbsp;Miao Yan ,&nbsp;Zhenming Zhang ,&nbsp;Bo Yu ,&nbsp;Zhaoying Li ,&nbsp;Shaohong Fang","doi":"10.1016/j.ncrna.2024.12.008","DOIUrl":"10.1016/j.ncrna.2024.12.008","url":null,"abstract":"<div><div>Acute coronary events show a diurnal rhythm, and atherosclerotic plaque vulnerability, as a histomorphological characteristic of major adverse cardiovascular events, is a key target for intervention. Although oscillating microRNAs reduce plaque stability by facilitating macrophage apoptosis in lesions, whether rhythmic long non-coding RNA (lncRNA) can regulate diurnal oscillations in plaque stability and the potential underlying mechanism remain unclear. In this study, we examined whether rhythmic lncRNAs are involved in the pathogenesis and progression of atherosclerosis and detected a novel circadian lncRNA-AK023617, which is positively correlated with the peak occurrence of major adverse cardiovascular events. Transfection of short interfering RNA specific to lnc-AK023617 into THP-1 cells dampened the oscillation of immunity-related GTPase family M protein 1 (Irgm1), which is negatively related to plaque stability. In ApoE^−/− mice fed a high-fat diet for 12 weeks, diurnal variations in lncAK023617 were consistent with the proportions of necroptotic cells in atherosclerotic plaques. In addition, reduced expression of lncAK023617 inhibited P-RIP3 and P-MLKL in THP-1 cells. Mechanistically, lncAK023617 interacted with the core molecular clock Bmal1 and promoted nuclear translocation of Bmal1, which could directly bind to the E-BOX elements in the <em>Irgm1</em> promoter. Thus, oscillating lncAK023617 in macrophages can affect plaque stability by regulating necroptosis, which regulates circadian expression of the target gene <em>Irgm1</em> by increasing the transcriptional activity of Bmal1, ultimately determining the diurnal oscillations in plaque stability. Therefore, lncAK023617 may serve as a specific target to ameliorate atherosclerotic plaque vulnerability.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 262-272"},"PeriodicalIF":5.9,"publicationDate":"2024-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11788686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143123785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lnc-RAINY regulates genes involved in radiation susceptibility through DNA:DNA:RNA triplex-forming interactions and has tumor therapeutic potential in lung cancers","authors":"Emily S. Westemeier-Rice ,&nbsp;Michael T. Winters ,&nbsp;Travis W. Rawson ,&nbsp;Kiran J. Patel ,&nbsp;Olivia McHugh ,&nbsp;Sierra Ward ,&nbsp;Sarah McLaughlin ,&nbsp;Amanda Stewart ,&nbsp;Bishal Misra ,&nbsp;Sebastian Dziadowicz ,&nbsp;Weijun Yi ,&nbsp;Sharan Bobbala ,&nbsp;Gangqing Hu ,&nbsp;Ivan Martinez","doi":"10.1016/j.ncrna.2024.12.004","DOIUrl":"10.1016/j.ncrna.2024.12.004","url":null,"abstract":"<div><div>Lung cancer is the leading cause of cancer related deaths worldwide. Unfortunately, radiation resistance remains a major problem facing lung cancer patients. Recently, we identified a group of long non-coding RNAs (lncRNAs) known as linc-SPRY3 RNAs, expressed on the Y-chromosome, which play a role in radiation sensitivity by decreasing tumor burden <em>in vitro</em> and <em>in vivo</em> after radiation. In this study, we found that the linc-SPRY3 RNAs are one large lncRNA that we named <em>Ra</em>diation <em>In</em>duced <em>Y</em>-chromosome linked long non-coding RNA (lnc-RAINY). Through ATAC-seq and immunoprecipitation experiments, we show that lnc-RAINY interacts with DNA in a triple helix to induce chromatin remodeling and gene expression. We also identified that lnc-RAINY regulates CDC6 and CDC25A expression affecting senescence induction, cell migration patterns, and cell cycle regulation. Furthermore, the administration of Lnc-RAINY encapsulated in FDA-approved nanoparticles into a lung cancer patient-derived xenograft model dramatically reduces tumor progression demonstrating therapeutic potential.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"12 ","pages":"Pages 152-166"},"PeriodicalIF":5.9,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143748432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA methylation of long noncoding RNA cytochrome B in diabetic retinopathy","authors":"Renu A. Kowluru,&nbsp;Jay Kumar,&nbsp;Pooja Malaviya","doi":"10.1016/j.ncrna.2024.12.007","DOIUrl":"10.1016/j.ncrna.2024.12.007","url":null,"abstract":"<div><div>Diabetic retinopathy, a microvascular complication of diabetes, is the leading cause of blindness in adults, but the molecular mechanism of its development remains unclear. Retinal mitochondrial DNA is damaged and hypermethylated, and mtDNA-encoded genes are downregulated. Expression of a long noncoding RNA (larger than 200 nucleotides, which does not translate into proteins), encoded by mtDNA, cytochrome B (Lnc<em>CytB</em>), is also downregulated. This study aims to investigate the role of DNA methylation in the downregulation of Lnc<em>CytB</em> in diabetic retinopathy. Human retinal endothelial cells, incubated in 5 mM (normal) or 20 mM (high) D-glucose, in the presence/absence of Azacytidine (a DNA methyl transferase inhibitor) were analyzed for Lnc<em>CytB</em> DNA methylation by immunoprecipitation and methylation specific PCR techniques, and Lnc<em>CytB</em> transcripts by strand-specific PCR and RNA-FISH. Mitochondrial genomic stability was evaluated by quantifying protective mtDNA nucleoids by SYBR green staining and by flow cytometry, and functional stability by oxygen consumption rate using Seahorse analyzer. Results were confirmed in an <em>in vivo</em> model using retina from diabetic rat. While high glucose elevated 5 mC and the ratio of methylated to unmethylated amplicons at Lnc<em>CytB</em> and downregulated its transcripts, azacytidine prevented Lnc<em>CytB</em> DNA hypermethylation and decrease in its expression. Azacytidine also ameliorated decrease in nucleoids and oxygen consumption rate. Similarly, azacytidine prevented increase in retinal Lnc<em>CytB</em> DNA methylation and decrease in its expression in diabetic rats. Thus, DNA hypermethylation plays a major role in the downregulation of retinal Lnc<em>CytB</em> in diabetes, resulting in impaired mitochondrial homeostasis, and culminating in the development of diabetic retinopathy.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 141-149"},"PeriodicalIF":5.9,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142984955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long non-coding RNA transcripts in Mycobacterium tuberculosis-host interactions","authors":"Mahalakshmi Vijayaraghavan ,&nbsp;Shrikanth S. Gadad ,&nbsp;Subramanian Dhandayuthapani","doi":"10.1016/j.ncrna.2024.12.005","DOIUrl":"10.1016/j.ncrna.2024.12.005","url":null,"abstract":"<div><div>Tuberculosis (TB) persists as a significant health threat, affecting millions of people all over the world. Despite years of control measures, the elimination of TB has become a difficult task as morbidity and mortality rates remain unaffected for several years. Developing new diagnostics and therapeutics is paramount to keeping TB under control. However, it largely depends upon understanding the pathogenic mechanisms of <em>Mycobacterium tuberculosis</em> (Mtb), the causative agent of TB. Mtb is an intracellular pathogen capable of subverting the defensive functions of the immune cells, and it can survive and multiply within humans' mononuclear phagocytes. Emerging evidence indicates that long non-coding RNAs (lncRNAs), a class of RNA molecules with limited coding potential, are critical players in this intricate game as they regulate gene expression at transcriptional and post-transcriptional levels and also by chromatin modification. Moreover, they have been shown to regulate cellular processes by controlling the function of other molecules, such as DNA, RNA, and protein, through binding with them. Recent studies have shown that lncRNAs are differentially regulated in the tissues of TB patients and cells infected in vitro with Mtb. Some dysregulated lncRNAs are associated with essential roles in modulating immune response, apoptosis, and autophagy in the host cells, adding a new dimension to TB pathogenesis. In this article, we provide a comprehensive review of the recent literature in this field and the impact of lncRNAs in unraveling pathogenic mechanisms in TB. We also discuss how the studies involving lncRNAs provide insight into TB pathogenesis, especially Mtb-host interactions.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 281-293"},"PeriodicalIF":5.9,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143129808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC00323 knockdown suppresses the proliferation, migration, and vascular mimicry of non-small cell lung cancer cells by promoting ubiquitinated degradation of AKAP1","authors":"Bin Ke ,&nbsp;Hai Zhong ,&nbsp;Yuxin Gong ,&nbsp;Xiaofei Chen ,&nbsp;Chenxin Yan ,&nbsp;Lin Shi","doi":"10.1016/j.ncrna.2024.12.006","DOIUrl":"10.1016/j.ncrna.2024.12.006","url":null,"abstract":"<div><h3>Background</h3><div>LINC00323, a new long noncoding RNA, is aberrantly expressed in several cancers. However, the expression, function, and mechanism of LINC00323 in non-small cell lung cancer (NSCLC) are unclear.</div></div><div><h3>Methods</h3><div>In the present study, LINC00323, VEGFA, microvessel density (MVD), and AKAP1 levels were confirmed in NSCLC tissues. Cell proliferation, migration, and vascular mimicry (VM) were examined to assess the effects of LINC00323 and AKAP1 on NSCLC cells. In addition, the interaction between LINC00323 and AKAP1 was verified by RNA pull-down, LC-MS/MS and RNA immunoprecipitation. The ubiquitination level of AKAP1 was also confirmed through coimmunoprecipitation, cycloheximide (CHX) chase, and ubiquitination assays in vitro.</div></div><div><h3>Results</h3><div>Our results revealed that LINC00323 was upregulated in NSCLC tissues and was positively correlated with metastasis, poor prognosis, VEGFA expression, elevated MVD, and AKAP1 expression. Functionally, LINC00323 or AKAP1 knockdown suppressed the proliferation, migration, and VM of NSCLC cells. Mechanistically, LINC00323 could target AKAP1, and LINC00323 knockdown accelerated ubiquitination-mediated AKAP1 protein degradation. Moreover, LINC00323 silencing suppressed NSCLC cell progression by downregulating AKAP1.</div></div><div><h3>Conclusions</h3><div>LINC00323 knockdown prevents NSCLC cell proliferation, migration, and VM formation by targeting AKAP1, indicating that LINC00323 and AKAP1 might be biological targets for NSCLC treatment.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 131-140"},"PeriodicalIF":5.9,"publicationDate":"2024-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11720444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting microRNA methylation: Innovative approaches to diagnosing and treating hepatocellular carcinoma","authors":"Albert Sufianov ,&nbsp;Murad Agaverdiev ,&nbsp;Andrey Mashkin ,&nbsp;Tatiana Ilyasova","doi":"10.1016/j.ncrna.2024.12.002","DOIUrl":"10.1016/j.ncrna.2024.12.002","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) stands as the most prevalent form of primary liver cancer and is frequently linked to underlying chronic liver conditions such as hepatitis B, hepatitis C, and cirrhosis. Despite the progress achieved in the field of oncology, HCC remains a significant clinical challenge, primarily due to its typically late-stage diagnosis and the complex and multifaceted nature of its tumor biology. These factors contribute to the limited effectiveness of current treatment modalities and result in poor patient prognosis. Emerging research has underscored the vital role of microRNAs (miRNAs)—small, non-coding RNA molecules that play a pivotal part in the post-transcriptional regulation of gene expression. These miRNAs are integral to a wide array of cellular functions, including proliferation, apoptosis, and differentiation, and their dysregulation is closely associated with the pathogenesis of various cancers, notably HCC. A major focus in recent studies has been on the epigenetic regulation of miRNAs through methylation, a key mechanism that modulates gene expression. This process, involving the addition of methyl groups to CpG islands in the promoter regions of miRNA genes, can result in either gene silencing or activation, influencing the expression of oncogenes and tumor suppressor genes. Such alterations have profound implications for tumor growth, metastasis, and resistance to treatment. Evidence suggests that aberrant miRNA methylation can serve as a powerful biomarker for early detection and prognosis in HCC and may present novel opportunities for therapeutic intervention. This review aims to provide a comprehensive overview of the current landscape of miRNA methylation in HCC, elucidating its significance in the molecular mechanisms of liver cancer and examining its potential for clinical application. By exploring the diagnostic and therapeutic potential of miRNA methylation, we seek to highlight its value in enhancing personalized treatment strategies and improving patient outcomes.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 150-157"},"PeriodicalIF":5.9,"publicationDate":"2024-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11742574/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143013428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}