Non-coding RNA Research最新文献

{"title":"Long noncoding RNA LINC00339 promotes osteoporosis development via modulating of regulator CDC42 by binding PARP1","authors":"Dong-Li Zhu ,&nbsp;Yan Zhang ,&nbsp;Xiao-Yu Zhang ,&nbsp;Zi-Han Qiu ,&nbsp;Ke Li ,&nbsp;Xiao-Rong Zhou ,&nbsp;Zhen-Zhen He ,&nbsp;Xiao-Feng Chen ,&nbsp;Shan-Shan Dong ,&nbsp;Wen Tian ,&nbsp;Ya-Kang Wang ,&nbsp;Tie-Lin Yang ,&nbsp;Bo Yang ,&nbsp;Yan Guo","doi":"10.1016/j.ncrna.2025.06.004","DOIUrl":"10.1016/j.ncrna.2025.06.004","url":null,"abstract":"<div><h3>Background</h3><div>Osteoporosis is a systemic skeletal disorder characterized by reduced bone mass and microarchitectural deterioration of bone tissue. Our previous investigation provided preliminary evidence that single nucleotide polymorphisms (SNPs) may functionally interact with the LINC00339, potentially contributing to the pathogenesis and progression of osteoporosis through undefined molecular pathways. However, the exact mechanistic basis of LINC00339's involvement in osteoporotic bone remodeling remains incompletely characterized and warrants systematic exploration.</div></div><div><h3>Methods</h3><div>We analyzed the differentially expressed of LINC003339 in different bone tissues by qRT-PCR. ALP and Alizarin red S (ARS) staining were conducted in stably knocked-down and overexpressed of LINC00339 cell lines. RNA fluorescence in situ hybridization (FISH) assays were used to detect the subcellular location of LINC00339. The mechanism of LINC00339 regulating cell division cycle 42 (CDC42) was explored by RNA-protein pull-down, RNA immunoprecipitation (RIP) and Co-IP assays.</div></div><div><h3>Results</h3><div>This study demonstrated significant upregulation of LINC00339 in bone tissue specimens derived from osteoporosis patients compared to healthy controls. Functional analyses revealed that LINC00339 dysregulation exhibited an inverse correlation with osteogenic differentiation capacity across multiple osteoblast cell models. Subcellular localization analysis via FISH confirmed the predominant cytoplasmic distribution of LINC00339 in bone cells. Mechanistically, RNA-protein pull-down assays combined with RNA immunoprecipitation (RIP) identified poly (ADP-Ribose) polymerase 1 (PARP1) as a direct binding partner of LINC00339. Further investigation established that the LINC00339-PARP1 axis cooperatively modulates transcriptional programs critical to bone homeostasis, potentially driving pathogenic mechanisms underlying osteoporosis progression. Notably, integrated transcriptomic and rescue experiments revealed that LINC00339 and PARP1 coregulate CDC42 expression through post-transcriptional regulatory mechanisms.</div></div><div><h3>Conclusions</h3><div>The identification of the LINC00339-PARP1-CDC42 regulatory axis elucidates a novel molecular mechanism contributing to osteoporosis pathogenesis. This discovery not only advances our understanding of epigenetic regulation in bone remodeling but also positions the LINC00339-PARP1 interaction as a potential therapeutic target for modulating osteoblast dysfunction. Importantly, these findings establish a conceptual framework for lncRNA-driven interventions in skeletal disorders, highlighting the translational potential of targeting RNA-protein complexes to restore bone homeostasis.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"15 ","pages":"Pages 18-28"},"PeriodicalIF":5.9,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144654332","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":"Serum lncRNAs NEAT1, PVT1 and H19 as novel biomarkers for sarcopenia diagnosis and treatment response","authors":"Paula Aparicio ,&nbsp;Tresa López-Royo ,&nbsp;David Navarrete-Villanueva ,&nbsp;Alba María Gómez Cabello ,&nbsp;Marcela González-Gross ,&nbsp;Ignacio Ara ,&nbsp;Germán Vicente-Rodríguez ,&nbsp;Rosario Osta ,&nbsp;Raquel Manzano","doi":"10.1016/j.ncrna.2025.06.003","DOIUrl":"10.1016/j.ncrna.2025.06.003","url":null,"abstract":"<div><div>Sarcopenia, the loss of muscle mass and function generally associated to age, leads to increased dependence and mortality in older adults. Despite its clinical significance, unclear molecular mechanisms hinder the development of universal diagnostic and therapeutic monitoring methods. Recent research suggests long non-coding RNAs (lncRNAs) as potential biomarkers for muscle damage and sarcopenia. This study investigates the role of six specific lncRNAs as biomarkers for diagnosing and monitoring sarcopenia following physical training. For this purpose, an initial cohort of participants was divided into two experiments: Trial 1, a cross-sectional study comprising 54 sarcopenic patients and 29 robust controls, both including men and women; Trial 2, a non-randomized controlled trial, where the same sarcopenic patients from Trial 1 were divided in two groups: a Control Group (CG, n = 15); and a Trained Group (TG, n = 22). RNA was extracted from serum samples for all the participants, and the expression of 6 lncRNA (PVT1, HOTAIR, MALAT1, NEAT1, GAS5, H19), selected from the literature, was quantified by RT-PCR and compared between the different groups. Statistical evaluation uncovered four lncRNAs with significantly distinct expression in Trial 1: PVT1 (LOG2FC = 1.194), GAS5 (LOG2FC = 0.8224), NEAT1 (LOG2FC = 1.497) and H19 (LOG2FC = −0.9958) and three lncRNA significantly different between TG and CG in Trial 2 (PVT1 (LOG2FC = −1.796), MALAT1 (LOG2FC = 2.834) and H19 (LOG2FC = 1.355). Among them, NEAT 1 stands aout as promissing diagnostic marker ans PVT1 and H19 may serve as both diagnosis and treatment monitoring, altough further validation in larger cohorts is needed to confirm these results.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"14 ","pages":"Pages 166-176"},"PeriodicalIF":5.9,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144548779","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":"Dual role of lncRNA OTUD6B-AS1 in immune evasion and ferroptosis resistance: A prognostic and therapeutic biomarker in breast cancer","authors":"Jia-Ning Zhang ,&nbsp;Zi-Lu Yi ,&nbsp;Xi-Rui Zhou ,&nbsp;Sha-sha Liu ,&nbsp;Hong Liu","doi":"10.1016/j.ncrna.2025.06.002","DOIUrl":"10.1016/j.ncrna.2025.06.002","url":null,"abstract":"<div><h3>Background</h3><div>Long non-coding RNAs (lncRNAs) have emerged as pivotal regulators in tumorigenesis and therapeutic resistance. This study investigates the prognostic significance and dual biological functions of lncRNA OTUD6B-AS1 in breast cancer (BC), focusing on its roles in immune evasion and ferroptosis resistance.</div></div><div><h3>Methods</h3><div>Multi-omics data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and lncRNA databases (AnnoLnc2, LncACTdb 3.0) were integrated to analyze OTUD6B-AS1 expression, clinical relevance, and molecular networks. Experimental validations included co-culture assays with CD8⁺ T cells, drug sensitivity tests, and ferroptosis marker analysis.</div></div><div><h3>Results</h3><div>OTUD6B-AS1 exhibited significant overexpression across multiple cancers, particularly in breast cancer (BC), where elevated levels strongly correlated with poor prognosis. Its expression was closely associated with key clinical indicators (T/N/M stage, ER/PR/HER2 status), prompting the development of a nomogram prognostic model with high clinical applicability. Genomic analysis revealed frequent amplification of OTUD6B-AS1 and co-occurrence of PIK3CA mutations. Co-expression and ceRNA networks highlighted its interaction with RNA degradation pathways. Notably, OTUD6B-AS1 was associated with immune evasion by regulating PD-L1 and CD8⁺ T cell activity. Concurrently, high OTUD6B-AS1 expression conferred ferroptosis resistance via GPX4/SLC7A11 modulation.</div></div><div><h3>Conclusion</h3><div>In conclusion, OTUD6B-AS1 serves as a biomarker in BC, driving immune evasion and ferroptosis resistance. Targeting OTUD6B-AS1 may enhance immunotherapy efficacy and overcome chemoresistance, offering novel therapeutic avenues.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"14 ","pages":"Pages 156-165"},"PeriodicalIF":5.9,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144489566","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 levels in the central nervous system as novel potential players and biomarkers in amyotrophic lateral sclerosis","authors":"Tresa López-Royo ,&nbsp;Laura Moreno-Martínez ,&nbsp;Gabriel Rada ,&nbsp;Sofía Macías-Redondo ,&nbsp;Ana Cristina Calvo ,&nbsp;Alberto García-Redondo ,&nbsp;Raquel Manzano ,&nbsp;Rosario Osta","doi":"10.1016/j.ncrna.2025.05.017","DOIUrl":"10.1016/j.ncrna.2025.05.017","url":null,"abstract":"<div><div>Research in amyotrophic lateral sclerosis (ALS) faces major burdens, including the urgent need for sensitive and specific biomarkers, the identification of novel and effective therapeutic targets and a deeper understanding of the mechanisms driving the disease. In this line, long non-coding RNAs (lncRNAs) have emerged as promising candidates due to their regulatory role in a variety of important biological processes such as RNA metabolism, neuroinflammation, apoptosis or proteostasis.</div><div>This study aims to elucidate the expression profile of 14 lncRNAs in both the SOD1^G93A mouse model and ALS patients. Different stages of the disease (presymptomatic, symptomatic and terminal) and 3 regions of the central nervous system (CNS) differentially affected by ALS (spinal cord, brainstem and frontal cortex) were included in the experimental design.</div><div>In SOD1^G93A mice, all 14 lncRNAs exhibited differential expression patterns influenced by sex, age, and region, except for Malat1, Neat1, and H19, which displayed consistent expression patterns (Malat1 was decreased, while Neat1 and H19 were increased). These patterns were most prominent in the spinal cord, where lncRNAs were overall down-regulated. In contrast, in the brainstem and frontal cortex, lncRNAs were predominantly up-regulated. Notably, <em>Gas5</em> expression levels in frontal cortex and spinal cord at the terminal stage correlated with the onset and progression of motor coordination and strength decline. Additionally, three lncRNAs (<em>Gas5</em>, <em>Neat1</em> and <em>Myoparr</em>) were found to significantly correlate with survival.</div><div>In human ALS samples, increased levels of <em>NEAT1</em> and <em>SNHG16</em> were observed in the brainstem, and of <em>MEG3</em> and <em>H19</em> in the frontal cortex, whereas <em>MALAT1</em> levels were decreased in frontal cortex.</div><div>In conclusion, this work supports lncRNAs as promising candidates as novel players and potential biomarkers in ALS and highlights SOD1^G93A mice as a good model to study lncRNAs in the CNS in the context of this disease.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"14 ","pages":"Pages 145-155"},"PeriodicalIF":5.9,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144471691","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":"Upregulation of LINC02154 promotes esophageal cancer progression by enhancing cell cycling and epithelial-mesenchymal transition","authors":"Kotoha Shimote ,&nbsp;Takeshi Niinuma ,&nbsp;Hiroshi Kitajima ,&nbsp;Kazuya Ishiguro ,&nbsp;Eiichiro Yamamoto ,&nbsp;Gota Sudo ,&nbsp;Akira Yorozu ,&nbsp;Mutsumi Toyota ,&nbsp;Masahiro Kai ,&nbsp;Masashi Idogawa ,&nbsp;Hiromu Suzuki","doi":"10.1016/j.ncrna.2025.06.001","DOIUrl":"10.1016/j.ncrna.2025.06.001","url":null,"abstract":"<div><div>Long noncoding RNAs (lncRNAs) play crucial roles in the progression of human malignancies; however, their involvement in esophageal cancer (ESCA) remains incompletely understood. In this study, we screened for lncRNAs upregulated in ESCA and identified 12 lncRNAs significantly upregulated in primary ESCA tumors. Among those, elevated LINC02154 expression correlated positively with advanced T stages. LINC02154 knockdown in ESCA cell lines suppressed cell proliferation and migration, while ectopic expression of LINC02154 enhanced colony formation. Depletion of LINC02154 suppressed genes involved in various oncogenic processes, including cell cycling, epithelial-mesenchymal transition (EMT), and metabolism. We also found that LINC02154 promotes EMT and enhances chemoresistance, at least in part, through suppression of miR-200b. Finally, RNA-pulldown and mass spectrometry analysis revealed that LINC02154 interacts with proteins involved in the cornified envelope or desmosome. These findings suggest that LINC02154 exerts oncogenic effects through modulation of multiple oncogenic signaling pathways in ESCA and that LINC02154 is a potential therapeutic target.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"14 ","pages":"Pages 107-116"},"PeriodicalIF":5.9,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144231637","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":"Deciphering the multifaceted role of circular RNA in aging: from molecular mechanisms to therapeutic potentials","authors":"Yang Wang ,&nbsp;Cong Wang ,&nbsp;Xin Dai ,&nbsp;Ge Liu ,&nbsp;Xiaolong Gao ,&nbsp;Junru Zhang","doi":"10.1016/j.ncrna.2025.05.015","DOIUrl":"10.1016/j.ncrna.2025.05.015","url":null,"abstract":"<div><div>Aging is an inevitable physiological process that occurs in living organisms and has significant implications for health and disease. As the human lifespan extends, the functionality of organs gradually diminishes, leading to the emergence of various aging-related symptoms. While it is not feasible to completely halt the aging process, investigating key molecules involved in aging can help devise valid strategies to delay its progression. Circular RNAs (circRNAs) are a novel category of non-protein-coding RNAs and are abundant in cells. Their distinctive circular structure and diverse biological functions have garnered considerable attention from the scientific community. CircRNAs play a crucial role in regulating biological processes such as the cell cycle, apoptosis, and autophagy. They are implicated in various mechanisms, including cell signaling, influencing post-transcriptional regulation, and functioning as sponges for microRNAs (miRNAs), to modulate gene expression and impact cellular senescence. This research paper sets out to elucidate the mechanisms by which circRNAs regulate gene expression, epigenetic modifications, and cellular functions, as well as to assess their potential applications in aging-associated disorders.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"14 ","pages":"Pages 129-144"},"PeriodicalIF":5.9,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144254875","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 MEG3/CTCF-CXCR4 axis functions in the regulation of breast cancer cell migration","authors":"Gusai Elhassan ,&nbsp;Xiangxue Bu ,&nbsp;Jiaxin Liu ,&nbsp;Shuai Hou ,&nbsp;Jinsong Yan ,&nbsp;Haixin Lei","doi":"10.1016/j.ncrna.2025.05.014","DOIUrl":"10.1016/j.ncrna.2025.05.014","url":null,"abstract":"<div><div>Loss or decreased expression of lncRNA MEG3 is a frequent event in the progression of many different malignancies. Overexpression of MEG3 in breast cancer cell lines MCF7 or MDA-MB-231 prevented cell migration, whereas depletion of MEG3 in human mammary epithelial cell line MCF10A strikingly promoted cell migration. As RNA-protein interactions are vital for RNA to function, RNP assembled on MEG3 <em>in vivo</em> was purified using affinity purification followed by mass spectrometry, which revealed ∼600 proteins with the potential to interact with MEG3. Bioinformatic analysis on RNA-seq data from MCF7 with MEG3 overexpression and MCF10A with MEG3 depletion led to the identification of CXCR4 as the major downstream mediator negatively regulated by MEG3 that facilitated breast cancer cell migration. In addition, the chromatin regulator CTCF emerged as the MEG3-binding protein that might regulate CXCR4 expression after comparison of proteins presenting in MEG3 lncRNP to ChIP-seq data and GPSAdb data of CXCR4. Further evidence was provided to show CTCF upregulated the expression of CXCR4 at transcriptional level, whereas co-expression of MEG3 with CTCF abolished transcriptional activation of CXCR4. Overall, our study pinpoints the importance of MEG3/CTCF-CXCR4 axis in regulating migration of breast cancer cells and provides novel insight into the mechanism of lncRNA MEG3 in cancer development.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"14 ","pages":"Pages 117-128"},"PeriodicalIF":5.9,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144241990","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":"MicroRNA-29a-5p attenuates hemorrhagic transformation and improves outcomes after mechanical reperfusion for acute ischemic stroke","authors":"Chang-Luo Li ,&nbsp;Jin-Kun Zhuang ,&nbsp;Zhong Liu ,&nbsp;Zhong-Run Huang ,&nbsp;Chun Xiang ,&nbsp;Qian-Yu Chen ,&nbsp;Ze-Xin Chen ,&nbsp;Zhong-Song Shi","doi":"10.1016/j.ncrna.2025.05.016","DOIUrl":"10.1016/j.ncrna.2025.05.016","url":null,"abstract":"<div><h3>Background</h3><div>Hemorrhage transformation (HT) following endovascular reperfusion treatment is associated with worse clinical outcomes in acute ischemic stroke patients. MicroRNA (miR) modulates several aspects of cerebral ischemia-reperfusion injury, including blood-brain barrier (BBB) integrity, inflammation, oxidative stress, and apoptosis, significantly impacting cerebral recovery and function. This study investigated the role of astrocytic miR-29a-5p in HT in the transient middle cerebral artery occlusion (MCAO) model and oxygen-glucose deprivation reoxygenation (OGD/R) model of astrocytes.</div></div><div><h3>Methods</h3><div>MiR-29a-5p expression in the OGD/R astrocyte model was assessed. The astrocyte injury, the expression of A1 and A2 phenotypes of reactive astrocytes, and the regulation of miR-29a-5p target genes were evaluated after the miR-29a-5p intervention. A mechanical reperfusion-induced HT model was established in hyperglycemic rats using 5-h MCAO following reperfusion at 6 h. MiR-29a-5p agomir was administered intravenously before reperfusion. Infarct volume, HT, BBB damage, neurological score, the expression of miR-29a-5p, and its target genes were evaluated.</div></div><div><h3>Results</h3><div>MiR-29a-5p expression decreased in OGD/R-treated astrocytes and the peri-infarction tissue and blood of the MCAO model. Elevating miR-29a-5p levels reduced astrocyte injury, suppressed neurotoxic A1 astrocyte markers (C3, Fkbp5, and Serping1), while enhanced neuroprotective A2 astrocyte markers (S100a10 and Emp1) in the OGD/R and MCAO models. Intravenous administration of miR-29a-5p agomir increased the expression of miR-29a-5p and reduced infarct volume, reperfusion-induced HT, and BBB breakdown after ischemia, improving neurological outcomes in the MCAO model. Overexpression of miR-29a-5p effectively suppressed the expression of its direct target genes, glycogen synthase kinase 3 beta and aquaporin 4 in the OGD/R and MCAO models.</div></div><div><h3>Conclusions</h3><div>MiR-29a-5p alleviates astrocyte injury and regulates A1 and A2 astrocyte markers, glycogen synthase kinase 3 beta, and aquaporin 4 in astrocytes subjected to ischemia-reperfusion injury. Astrocytic miR-29a-5p may be a protective target for reducing HT and improving outcomes following mechanical reperfusion in acute ischemic stroke.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"14 ","pages":"Pages 96-106"},"PeriodicalIF":5.9,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144231636","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":"LncPTEN1, a long non-coding RNA generated from PTEN, suppresses lung cancer metastasis through the regulation of EMT progress","authors":"Zichu Shen ,&nbsp;Ailin Zhong ,&nbsp;Chun Zhang ,&nbsp;Xiaowei Tang ,&nbsp;Xuyang Zhao ,&nbsp;Zhiyuan Hou ,&nbsp;Hui Liang ,&nbsp;Yuxin Yin","doi":"10.1016/j.ncrna.2025.05.011","DOIUrl":"10.1016/j.ncrna.2025.05.011","url":null,"abstract":"<div><div>Lung cancer is among the most frequently observed and lethal malignancies globally, and metastasis represents a critical determinant of patient outcomes. PTEN, a well-established tumor suppressor, has emerged as an important regulator in lung cancer progression. However, the molecular mechanism of <em>PTEN</em> gene suppressing lung cancer metastasis lacks deeper exploration. In this research, we identify and characterize LncPTEN1, a novel long non-coding RNA generated from <em>PTEN</em> gene. We show that YTHDC1 promotes the alternative splicing of LncPTEN1, resulting in significantly elevated LncPTEN1 expression in normal lung cells. Clinical analyses across multiple patient cohorts demonstrate that low LncPTEN1 expression strongly correlates with poor patient survival and increased metastasis, indicating its potential as a prognostic biomarker. Mechanistically, LncPTEN1 facilitates the interaction between Trim16 and Vimentin, promoting the ubiquitination and proteasomal degradation of Vimentin, thereby suppressing EMT-driven metastasis. The collective evidence from our investigation demonstrates that LncPTEN1 represents a novel tumor-suppressive lncRNA which inhibits lung cancer metastasis through promoting the degradation of Vimentin and inhibiting the EMT progress.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"14 ","pages":"Pages 25-37"},"PeriodicalIF":5.9,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144203875","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 multifaceted role of microRNAs in colorectal cancer: pathogenesis and therapeutic implications","authors":"Federica Longo ,&nbsp;Giuseppe Gattuso ,&nbsp;Graziana Spoto ,&nbsp;Daria Ricci ,&nbsp;Anastasia Cristina Venera Vitale ,&nbsp;Alessandro Lavoro ,&nbsp;Saverio Candido ,&nbsp;Massimo Libra ,&nbsp;Luca Falzone","doi":"10.1016/j.ncrna.2025.05.012","DOIUrl":"10.1016/j.ncrna.2025.05.012","url":null,"abstract":"<div><div>MicroRNAs (miRNAs) are important regulators of gene expression and their dysregulation is involved in various diseases, including tumors. Among these, colorectal cancer (CRC) is the result of both genetic and epigenetic alterations with miRNAs playing a key pathogenetic role. Although numerous studies have investigated the most frequently dysregulated miRNAs in CRC, there is still no consensus on the specific role of individual miRNAs in the mechanisms leading to tumorigenesis, tumor progression, and the development of chemoresistance. This lack of clarity highlights the need for a deeper understanding of miRNA functions in CRC. Therefore, this review aims to clarify the role of miRNAs in CRC by examining their involvement in major oncogenic pathways, highlighting key miRNAs implicated in the disease, and exploring their potential as diagnostic biomarkers and therapeutic targets. By providing a comprehensive overview, we hope to shed light on the complex and multifaceted roles of miRNAs in CRC, which could pave the way for more effective CRC monitoring and the development of miRNA-guided therapeutic strategies.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"14 ","pages":"Pages 65-95"},"PeriodicalIF":5.9,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144220903","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}