Non-coding RNA Research最新文献

{"title":"SNHG5 enhances colorectal cancer metastasis through RNA–protein interaction with GNB2 and activation of canonical Wnt signaling","authors":"Xinyi Chen ,&nbsp;Mu Yang ,&nbsp;Xiaoxiao Luo,&nbsp;Xianglin Yuan","doi":"10.1016/j.ncrna.2025.12.002","DOIUrl":"10.1016/j.ncrna.2025.12.002","url":null,"abstract":"<div><h3>Background and purpose</h3><div>Colorectal cancer (CRC) is one of the most prevalent and lethal malignancies worldwide, with distant metastasis—particularly to the liver—representing the primary cause of poor prognosis. Long non-coding RNAs (lncRNAs) have emerged as critical regulators of CRC progression, yet the mechanisms by which they modulate G protein signaling during hepatic metastasis remain unclear. This study aimed to determine the role of the lncRNA SNHG5 in CRC liver metastasis and to explore whether G protein–related mechanisms are involved in this process.</div></div><div><h3>Methods</h3><div>We established murine MC38 CRC sublines with distinct metastatic capacities (F0 and F3) and performed RNA sequencing to identify key lncRNAs. Biotin-labeled RNA pull-down coupled with mass spectrometry was used to identify SNHG5-interacting proteins. The SNHG5–GNB2 interaction was validated using RIP, RNA-FISH, and Western blot analyses. Functional rescue assays, in vivo liver metastasis models, and Wnt pathway activity measurements were conducted to delineate downstream effects. Public transcriptomic datasets from GEO and TCGA were used to assess the expression patterns and prognostic relevance of SNHG5 and GNB2 in CRC and metastatic lesions.</div></div><div><h3>Results</h3><div>SNHG5 was significantly upregulated in the highly metastatic F3 subline and predominantly localized in the cytoplasm. Pull-down and proteomic analysis identified GNB2, a classical G protein β-subunit, as a direct binding partner of SNHG5. Functionally, SNHG5 promoted cell proliferation, migration, epithelial–mesenchymal transition (EMT), and suppressed apoptosis, while GNB2 overexpression partially rescued the tumor-suppressive phenotypes induced by SNHG5 silencing. Mechanistically, the SNHG5–GNB2 axis enhanced Wnt/β-catenin signaling via increased p-GSK3β and β-catenin levels, thereby driving EMT. Transcriptomic analyses further revealed that GNB2 is upregulated in CRC and liver metastases and is associated with poor prognosis. Multi-omics data suggested additional roles for this axis in immune evasion, metabolic reprogramming, and remodeling of the metastatic microenvironment.</div></div><div><h3>Conclusion</h3><div>This study provides the first evidence that SNHG5 promotes CRC liver metastasis through direct interaction with GNB2 and subsequent activation of the Wnt/β-catenin pathway. The SNHG5–GNB2 axis orchestrates a multilayered regulatory network that integrates EMT induction, immune suppression, and metabolic adaptation, highlighting its potential as a mechanistic driver and therapeutic target in metastatic CRC.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"17 ","pages":"Pages 128-149"},"PeriodicalIF":4.7,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145884388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic H3K4me3 activation of miR-155-5p promotes intervertebral disc degeneration via autophagy and ageing in nucleus pulposus cells","authors":"Ximeng Wang ,&nbsp;Hanqiu Sun ,&nbsp;Wenbiao Xiao ,&nbsp;Yuxuan Zhang ,&nbsp;Xiao Lu ,&nbsp;Zhaoyang Gong ,&nbsp;Dachuan Li ,&nbsp;Siyang Liu ,&nbsp;Xinlei Xia ,&nbsp;Hongli Wang ,&nbsp;Minghao Shao ,&nbsp;Guangyu Xu ,&nbsp;Xiaosheng Ma","doi":"10.1016/j.ncrna.2025.12.001","DOIUrl":"10.1016/j.ncrna.2025.12.001","url":null,"abstract":"<div><div>Nucleus pulposus (NP) cell ageing and impaired autophagy - lysosome biogenesis (ALB) are key drivers of intervertebral disc degeneration (IVDD). The upstream epigenetic regulation of transcription factor EB (TFEB), a major ALB regulator, remains elusive. Our study identifies a H3K4me3-associated miRNA pathway that modulates TFEB activity and IVDD progression. Using <em>in vivo</em> and <em>in vitro</em> models, we found that methyltransferase MLL3 knockdown reduces H3K4me3 methylation at the miR-155-5p promoter, suppressing miR-155-5p transcription. MiR-155-5p directly targets FBXO22, indirectly repressing TFEB transcription and exacerbating NP cells ageing and IVDD. Notably, experiments confirmed MLL3 binds specifically to the miR-155-5p promoter, with no interaction detected at the TFEB or FBXO22 promoters. Our data establish a linear H3K4me3/miR-155-5p/FBXO22/TFEB axis in IVDD pathogenesis. We reveal a novel epigenetic crosstalk where H3K4me3 methylation mediates miRNA-driven TFEB regulation, independent of canonical mTOR signaling. These findings enhance understanding of epigenetic mechanisms in autophagy and ageing control and highlight MLL3 and miR-155-5p as potential IVDD therapeutic targets.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"17 ","pages":"Pages 112-127"},"PeriodicalIF":4.7,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145840625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The crosstalk network of non-coding RNAs: Emerging opportunities for the clinical application of osteoporosis","authors":"Chunlu Yan ,&nbsp;Qiao Wan ,&nbsp;Zeling Fang ,&nbsp;Chuangwei Sui ,&nbsp;Xiaolong Xiao ,&nbsp;Fan Yang ,&nbsp;Baoshan Di ,&nbsp;Yajun Li ,&nbsp;Juan Yu ,&nbsp;Yana Zhao ,&nbsp;Guoliang Liu ,&nbsp;Yibo Zhou ,&nbsp;Wei Li ,&nbsp;Fangyu An","doi":"10.1016/j.ncrna.2025.11.008","DOIUrl":"10.1016/j.ncrna.2025.11.008","url":null,"abstract":"<div><div>Current methods for testing bone density lack the capability to detect patients with early bone loss, and existing osteoporosis therapies have limitations in their efficacy and safety. Therefore, the development of more precise and convenient diagnostic technologies and novel treatments is of paramount importance. Extracellular vesicle (EV)-mediated non-coding RNA (ncRNA) interaction networks enable both the detection of early bone loss and targeted therapy for enhanced treatment outcomes. In this review, we highlight the utility of EVs for carrying various ncRNAs (e.g., miRNAs, lncRNAs, and circRNAs) and thereby forming a complex regulatory network amongst bone-related cells such as osteoblasts and osteoclasts. The mechanisms through which EVs regulate bone cells and their potential for clinical translation are described in detail. Although the EV-mediated ncRNA network holds great promise for the precise diagnosis and targeted treatment of osteoporosis, rigorous large-scale studies are still required to address challenges related to its specificity and clinical application.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"17 ","pages":"Pages 90-111"},"PeriodicalIF":4.7,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145797814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hsa_circ_0101645 contributes to excessive autophagy and apoptosis in intervertebral disc degeneration by acting as a miR-1304-5p sponge modulating BNIP3 expression","authors":"Jianhai Luo ,&nbsp;Tong Yu ,&nbsp;Pengcheng Hu ,&nbsp;Jie Liu","doi":"10.1016/j.ncrna.2025.11.007","DOIUrl":"10.1016/j.ncrna.2025.11.007","url":null,"abstract":"<div><h3>Background</h3><div>Intervertebral disc (IVD) degeneration (IVDD) is the pathological foundation and principal cause for degenerative spine related diseases. Currently, its molecular pathogenesis and reliable biomarkers remain poorly understood. This study intends to elucidate the potential molecular mechanisms of circular RNAs (circRNAs) in IVDD, and to identify novel targeted therapeutic strategies.</div></div><div><h3>Methods</h3><div>Differentially expressed circRNAs (DE-circRNAs) were obtained by a secondary analysis of the IVDD-related dataset GSE67566, followed by enrichment analysis of their host genes. Both <em>in vitro</em> mechanical loading-induced and <em>in vivo</em> tail suspension-induced models were applied to validate the functions of hsa_circ_0101645, miRNA-1304-05p, and BCL2 Interacting Protein 3 (BNIP3) in IVDD. The competing endogenous RNA (ceRNA) mechanism involving hsa_circ_0101645/miR-1304-5p/BNIP3 was authenticated using dual luciferase reporter genes, Argonaute2-RNA binding protein immunoprecipitation, and RNA-RNA pull down.</div></div><div><h3>Results</h3><div>In the bioinformatics, there were 354 significantly down-regulated and 282 up-regulated DE-circRNAs in IVDD. The host genes of these circRNAs were mainly enriched in cell morphogenesis, autophagy, and apoptosis. In clinical samples, hsa_circ_0101645 in DE-circRNAs was markedly overexpressed in endplate chondrocytes (EPC) derived from IVDD patients and was predominantly localized in the cytoplasm. <em>In vitro</em>, overexpression of hsa_circ_0101645 and BNIP3, or knockdown of miR-1304-5p, dramatically diminished EPC viability and enlarged apoptosis and autophagic flux. <em>In vivo</em>, sa_circ_0101645 knockdown alleviated structural collapse and tissue lesions in the cartilage endplates, nucleus pulposus and annulus fibrosus of the IVD. Mechanistically, Hsa_circ_0101645 upregulated BNIP3 expression by serving as miR-1304-5p sponge.</div></div><div><h3>Conclusions</h3><div>Hsa_circ_0101645 service as ceRNA that facilitates IVDD process by mediating proliferation, apoptosis, and excessive autophagy of CEP via the miR-1304-5p/BNIP3 axis. These findings suggest that hsa_circ_0101645 represents a promising molecular target for IVDD therapy.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"17 ","pages":"Pages 76-89"},"PeriodicalIF":4.7,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145797815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"circ_0103896/miR-432–5p/FTO feedback loop suppresses the formation and progression of intracranial aneurysm","authors":"Zhiwen Lu ,&nbsp;Shijie Zhu ,&nbsp;Yina Wu ,&nbsp;Fengfeng Xu ,&nbsp;Qinghai Huang","doi":"10.1016/j.ncrna.2025.11.001","DOIUrl":"10.1016/j.ncrna.2025.11.001","url":null,"abstract":"<div><div>Circular RNAs (circRNAs) and m⁶A RNA methylation play crucial roles in the pathogenesis of intracranial aneurysm (IA); however, their regulatory interplay remains unclear. Through circRNA profiling of 16 IA tissues and 8 superficial temporal arteries, we identified hsa_circ_0103896 as significantly downregulated in IA. RT-qPCR analysis further revealed that decreased circ_0103896 or increased miR-432–5p expression correlated with IA progression. Functional assays demonstrated that circ_0103896 inhibited the phenotypic switch of human brain vascular smooth muscle cells (hBVSMCs) from a contractile to a synthetic state, whereas circ_0103896 knockdown reversed this effect. <em>In vivo</em>, circ_0103896 overexpression alleviated IA severity, whereas its depletion aggravated aneurysm formation. Mechanistically, circ_0103896 functioned as a sponge for miR-432–5p, thereby upregulating FTO, which in turn promoted m⁶A demethylation of circ_0103896. This process reinforced circ_0103896 expression, forming a positive feedback loop. The circ_0103896/miR-432–5p/FTO axis thus suppresses hBVSMC phenotypic transformation and mitigates IA progression. These findings reveal a novel epigenetic mechanism involving m⁶A modification and circRNA–miRNA crosstalk in IA pathogenesis, highlighting circ_0103896 as a potential therapeutic target.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"17 ","pages":"Pages 59-75"},"PeriodicalIF":4.7,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145797816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA ZFAS1 in hepatocellular carcinoma: A systematic review of molecular mechanisms and clinical translation","authors":"Peng Zhu ,&nbsp;Hui-ying Liu","doi":"10.1016/j.ncrna.2025.11.003","DOIUrl":"10.1016/j.ncrna.2025.11.003","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality globally, with its high recurrence rate and therapeutic resistance underscoring the urgent need for breakthrough molecular targets. The long non-coding RNA ZFAS1 has emerged as a critical regulatory hub in HCC pathogenesis through its multidimensional mechanisms. Clinical investigations reveal significant ZFAS1 overexpression in HCC tissues, which is strongly associated with microvascular invasion, lymph node metastasis, and unfavorable clinical outcomes. Meta-analytical data further corroborate its independent prognostic value in survival prediction.</div><div>Mechanistically, ZFAS1 functions as a competitive endogenous RNA (ceRNA) that sequesters tumor-suppressive miRNAs including miR-150 and miR-193a-3p, thereby de-repressing downstream oncogenic targets such as ZEB1/MMP14 and RALY/HGF/c-Met. This molecular interplay drives epithelial-mesenchymal transition (EMT) and metastatic progression, while ZFAS1-encoded micropeptides concurrently inhibit ferroptosis through mitochondrial ROS modulation and the miR-150/AIFM2 axis, thereby synergistically enhancing tumor proliferation and apoptotic resistance. Within the tumor microenvironment (TME), exosome-derived ZFAS1 remodels intercellular communication networks, promoting angiogenesis via STAT3/VEGFA signaling, though its immunometabolic regulatory mechanisms warrant further elucidation. Clinically, plasma ZFAS1 demonstrates enhanced diagnostic utility when combined with alpha-fetoprotein (AUC = 0.891), while therapeutic targeting of ZFAS1-mediated PI3K-AKT and PERK/ATF4 pathways shows promise in overcoming sorafenib/donafenib resistance. Current translational challenges include ZFAS1 isoform heterogeneity, suboptimal liquid biopsy sensitivity, and dynamic TME interactions.</div><div>Future directions should employ multi-omics integration (spatial transcriptomics/single-cell sequencing) coupled with AI-driven network modeling to systematically decode ZFAS1's regulatory architecture, ultimately enabling precision theranostic strategies for HCC management.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"17 ","pages":"Pages 44-53"},"PeriodicalIF":4.7,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145692651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TPR is required for circRNA, lncRNA and mRNA nuclear export","authors":"Min Zhou ,&nbsp;Ruirui Jia ,&nbsp;Mengya Gao ,&nbsp;Jun Yang ,&nbsp;Hongbo Qi","doi":"10.1016/j.ncrna.2025.11.010","DOIUrl":"10.1016/j.ncrna.2025.11.010","url":null,"abstract":"<div><h3>Background</h3><div>Efficient RNA nuclear export is essential for proper cellular function and normal physiology, with defects in this process leading to pathological consequences. Our study aimed to investigate the role of translocated promoter region (TPR), nuclear basket protein, in orchestrating RNA transport in human cells as well as the function of TPR-mediated RNA nuclear export in cervical cancer cells.</div></div><div><h3>Methods</h3><div>RNA sequencing and bioinformatic analysis were applied to explore the effect of TPR on circular RNAs (circRNAs), long non-coding RNAs (lncRNAs), and mRNAs nuclear export and their corresponding sequence characteristic. Fluorescence in situ hybridization was employed to explore the role of TPR in RNA nuclear export. Immunofluorescence staining was used to study the role of TPR in R-loop and DNA damage. Flow cytometry assay was applied to investigate the influence of TPR on cell cycle in cervical cancer cells.</div></div><div><h3>Results</h3><div>TPR depletion leads to the nuclear accumulation of 7243 circRNAs, 1913 lncRNAs, and 2758 mRNAs. Codepletion and rescue experiments suggested that the modulation of TPR-mediated circRNAs nuclear export might be independent of XPO4. The regulation of TPR-mediated circRNAs nuclear export is independent of circRNAs characteristics, while, the regulation of TPR-mediated lncRNAs and mRNAs nuclear export is partly dependent on lncRNAs/mRNAs transcription length. Moreover, the lack of TPR results in nuclear R-loop accumulation, causing DNA damage and cell cycle arrest as well as subsequent inhibition of cell proliferation in cervical cancer cells.</div></div><div><h3>Conclusions</h3><div>This study highlights the nuclear export of circRNA, lncRNA and mRNA relies critically on TPR, a mechanism that may inhibit nuclear accumulation of R-loop and DNA damage in cervical cancer cells.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"17 ","pages":"Pages 32-43"},"PeriodicalIF":4.7,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145692652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The regulatory role of circGDI2 in hepatocellular carcinoma proliferation and glycolysis with the involvement of m6A modification","authors":"Shiyi Chen ,&nbsp;Hongxiang Xia ,&nbsp;Shuwei Chen","doi":"10.1016/j.ncrna.2025.11.006","DOIUrl":"10.1016/j.ncrna.2025.11.006","url":null,"abstract":"<div><h3>Background</h3><div>Hepatocellular carcinoma (HCC) is a highly aggressive malignancy, and metabolic reprogramming, particularly glycolysis, plays a crucial role in its progression. Circular RNAs (circRNAs) and N6-methyladenosine (m⁶A) modifications have emerged as key regulators in HCC, but the role of circGDI2 and its underlying mechanisms remain unclear.</div></div><div><h3>Objective</h3><div>This study aimed to investigate the functional role and mechanism of circGDI2 in HCC proliferation and glycolysis.</div></div><div><h3>Methods</h3><div>The expression of circGDI2 was detected by RT-qPCR. RNase R treatment was used to verify the stability of circGDI2. Functional assays, including CCK-8, glycolysis analysis (glucose consumption, lactate production), and xenograft model, were performed to assess proliferation and glycolysis. Bioinformatics prediction, MeRIP, and luciferase reporter assays were used to explore the interaction between circGDI2, IGF2BP2, and PKM2.</div></div><div><h3>Results</h3><div>CircGDI2 was highly expressed in HCC tissues and cells, and exhibited cytoplasm localization. Silencing circGDI2 inhibited Li-7 and Huh-7 cell proliferation and glycolysis, downregulated PKM2, and suppressed tumor growth. Mechanistically, circGDI2 regulated PKM2 through the m⁶A “reader” IGF2BP2, and its overexpression partially rescued the inhibitory effects of circGDI2 knockdown. Furthermore, FTO-mediated m⁶A modification enhanced circGDI2 stability and expression. Silencing FTO inhibited HCC cell proliferation, glycolysis, and tumor growth, and decreased the levels of circGDI2, IGF2BP2, and PKM2.</div></div><div><h3>Conclusions</h3><div>FTO-mediated m⁶A modification of circGDI2 promotes HCC proliferation and glycolysis via the IGF2BP2/PKM2 axis, suggesting circGDI2 as a potential therapeutic target for HCC.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"17 ","pages":"Pages 21-31"},"PeriodicalIF":4.7,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145692670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circular RNA MALAT1 as a potential target for antimetastatic therapy","authors":"Janusz Matuszyk","doi":"10.1016/j.ncrna.2025.11.004","DOIUrl":"10.1016/j.ncrna.2025.11.004","url":null,"abstract":"<div><div>Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1) is a long non-coding RNA (lncRNA) located in the nucleus that is involved in the regulation of gene expression and alternative splicing of gene transcription products. MALAT1 has also been implicated in processes leading to metastasis in various types of cancer. On the other hand, during the epithelial-to-mesenchymal transition (EMT) process of cancer cells, which allows the invasion and migration of cancer cells outside the primary tumor, increases in the levels of the Quaking RNA-binding protein (QKI) were found, which also led to the formation of circular RNA molecules (circRNA), including <em>MALAT1</em>-derived circRNAs. It was also found that at least some <em>MALAT1</em>-derived circRNAs could support processes leading to the spread of cancer cells outside the primary tumor. Due to the unique back-splicing junction in a given circRNA, it is possible to therapeutically target specific circRNA molecules in cancer cells while protecting linear RNAs in normal cells. Without questioning the aberrant involvement of lncRNA MALAT1 in promoting cancer cell migration and invasion, it appears that <em>MALAT1</em>-derived circRNAs, especially the circRNA known as circ-MALAT1 or circ2082 (hsa_circ_0002082), among other circRNAs, may be considered for further study as potential targets for anti-metastatic therapy.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"17 ","pages":"Pages 12-20"},"PeriodicalIF":4.7,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145692671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The progress of m6A methylation-regulated non-coding RNAs in osteogenic differentiation and osteoporosis","authors":"Yongbin Wang ,&nbsp;Baicheng Ma ,&nbsp;Jiashuo Qiu ,&nbsp;Likun Yu ,&nbsp;Jianjun Xiong ,&nbsp;Qianfu Yu ,&nbsp;Xingnuan Li ,&nbsp;Haichun Liao ,&nbsp;Youen Huang ,&nbsp;Shan He","doi":"10.1016/j.ncrna.2025.11.005","DOIUrl":"10.1016/j.ncrna.2025.11.005","url":null,"abstract":"<div><div>N6-methyladenosine (m6A) is the most abundant internal modification of eukaryotic RNA, and has increasingly been recognized as a critical regulator of gene expression at both the transcriptional and post-transcriptional levels. The m6A modification process is highly dynamic and reversible, governed by methyltransferase writers (e.g., METTL3, METTL14, WTAP), demethylase erasers (such as FTO and ALKBH5), and specific readers (including YTHDF and IGF2BP protein families) that interpret the modification and mediate its downstream effects. Accumulating evidence indicates that m6A-mediated regulation of non-coding RNAs (ncRNAs) plays a pivotal role in osteogenic differentiation, a process central to bone formation. Impaired osteogenesis, which contributes to decreased bone mass, is closely linked to the onset and progression of osteoporosis. This review summarizes recent progress on the interplay between m6A modification and ncRNAs in osteogenic differentiation, and outlines a regulatory framework, the m6A-ncRNA-target gene axis, that includes m6A modification, ncRNA interactions, and downstream signaling pathways, such as Wnt/β-catenin and BMP/Smad, and discusses their potential as biomarkers or therapeutic targets for osteoporosis, with the goal of providing new insights into the epigenetic mechanisms underlying osteoporosis and to identify potential molecular targets for future therapeutic strategies.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"17 ","pages":"Pages 1-11"},"PeriodicalIF":4.7,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145645799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}