Non-coding RNA Research最新文献

{"title":"MicroRNA-541-3p/Rac2 signaling bridges radiation-induced lung injury and repair","authors":"Jiandong Zhang ,&nbsp;Lei Ma ,&nbsp;Limin He ,&nbsp;Quanxiao Xu ,&nbsp;Yan Ding ,&nbsp;Lidong Wang","doi":"10.1016/j.ncrna.2025.01.010","DOIUrl":"10.1016/j.ncrna.2025.01.010","url":null,"abstract":"<div><h3>Background</h3><div>While radiation-induced lung injury decreases quality of life and suppresses efficacy of radiotherapy, to date, the relationship between radiation-induced lung injury and repair remains unclear. Our previous studies revealed that TNFRSF10B-RIPK1/RIPK3-MLKL signaling induces necroptosis of alveolar epithelial cells and potentiates radiation-induced lung injury. We also found that microRNA-541-3p is differentially expressed in radiation-damaged lungs. The connection between microRNA-541-3p, TNFRSF10B signaling, and TGFβ1 signaling is also unclear.</div></div><div><h3>Objective</h3><div>This study was performed to explore the regulatory effects of microRNA-541-3p on TNFRSF10B and TGFβ1 signaling.</div></div><div><h3>Methods</h3><div>Mouse alveolar epithelial cells were transfected with a vector expressing microRNA-541-3p to regulate expression of target genes. Flow cytometry, polymerase chain reaction, and western blotting were used to analyze cell necroptosis, target gene expression, and target protein expression, respectively.</div></div><div><h3>Results</h3><div>Overexpression of microRNA-541-3p positively regulated TNFRSF10B-RIPK1/RIPK3-MLKL signaling through Rac2 to induce cell necroptosis. MicroRNA-541-3p negatively regulates Rac2. MicroRNA-541-3p and Rac2 regulate the expression of Tgf-beta1 and its encoded proteins.</div></div><div><h3>Conclusions</h3><div>The Rac2 gene synchronously regulates TNFRSF10B-RIPK1/RIPK3-MLKL and TGFβ1 signaling. MicroRNA-541-3P/Rac2 act as mediators of radiation damage and repair signaling.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"12 ","pages":"Pages 10-19"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143379378","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 ANRIL/p65 negative feedback loop protects intestinal barrier function in inflammatory bowel disease","authors":"Keqi Yu ,&nbsp;Hong Peng ,&nbsp;Zhechuan Zhang ,&nbsp;Lu Ye ,&nbsp;Ke Zhan ,&nbsp;Chuanfei Li ,&nbsp;Li Gan ,&nbsp;Yuru Lin ,&nbsp;Yanhui Wang ,&nbsp;Ya Song ,&nbsp;Zhechuan Mei ,&nbsp;Shengtao Liao ,&nbsp;Jinjun Guo ,&nbsp;Lin Lv","doi":"10.1016/j.ncrna.2025.03.002","DOIUrl":"10.1016/j.ncrna.2025.03.002","url":null,"abstract":"<div><div>Patients with inflammatory bowel disease (IBD) demonstrate varying expression levels of long non-coding RNAs (lncRNAs) in their intestinal mucosa, which can potentially impact the function of the intestinal barrier. This impact may occur through the modulation of epithelial cell apoptosis, alteration of intestinal mucosal barrier permeability, and enhancement of inflammatory responses. The objective of this study was to explore the role and underlying mechanisms of the downregulated lncRNA ANRIL in modulating intestinal barrier function in IBD. Notably, ANRIL was found to be significantly downregulated in patients diagnosed with ulcerative colitis (UC), correlating strongly with disease progression. The overexpression of ANRIL in mice treated with dextran sulfate sodium (DSS) resulted in a significant reduction in colonic damage. This was accompanied by the suppression of pro-inflammatory cytokines such as IL-6, TNF-α, and IL-1β, and an improvement in intestinal barrier function. Transcriptome sequencing following overexpression of ANRIL revealed a significant enrichment of the NF-κB signaling pathway. In both DSS-induced mouse colitis and LPS-induced FHC cell models, the upregulation of ANRIL effectively suppressed the activation of the NF-κB pathway. Furthermore, our findings demonstrated that ANRIL competes with YY1 for binding, thereby inhibiting the interaction between YY1 and p65 subunit of NF-κB. This disruption in interaction results in the suppression of transcriptional activation of NF-κB p65, leading to a reduced expression of inflammatory cytokines and the promotion of intestinal barrier function in IBD.Additionally, we identified a negative feedback loop involving ANRIL and p65, wherein p65 binds to the ANRIL promoter, promoting ANRIL expression. In summary, the ANRIL/p65 negative feedback loop represents a potential therapeutic target for protecting intestinal barrier function in IBD.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"12 ","pages":"Pages 167-179"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143767682","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":"Development of a microRNA-Based age estimation model using whole-blood microRNA expression profiling","authors":"Yanfang Lu ,&nbsp;Anqi Chen ,&nbsp;Mengxiao Liao ,&nbsp;Ruiyang Tao ,&nbsp;Shubo Wen ,&nbsp;Suhua Zhang ,&nbsp;Chengtao Li","doi":"10.1016/j.ncrna.2025.03.003","DOIUrl":"10.1016/j.ncrna.2025.03.003","url":null,"abstract":"<div><div>Age estimation is a critical aspect of human identification. Traditional methods, reliant on morphological examinations, are often suitable for living subjects. However, there are relatively few studies on age estimation based on biological samples, such as blood. Recent advancements have concentrated on DNA methylation for forensic age prediction. However, to explore further possibilities, this study investigated microRNAs (miRNAs) as alternative molecular markers for age estimation. Peripheral blood samples from 127 healthy individuals were analyzed for miRNA expression using small RNA sequencing. Lasso regression selected 103 candidate miRNAs, and Shapley additive explanations (SHAP) analysis identified 38 key miRNAs significant for age prediction. Five machine learning models were developed, with the elastic net model achieving the best performance (MAE of 4.08 years) on the testing set, surpassing current miRNA age estimation results. Additionally, we observed significant changes in the expression levels of miRNAs in healthy individuals aged 48–52 years. This study demonstrated the potential of blood miRNA biomarkers in age prediction and provides a set of miRNA markers for developing more accurate age prediction methods.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"12 ","pages":"Pages 81-91"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143577509","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":"Corrigendum to “piR-36249 and DHX36 together inhibit testicular cancer cells progression by upregulating OAS2” [Noncoding RNA Research 2023 8 (2) 174–186]","authors":"Qianqian Wang ,&nbsp;Peize Chen ,&nbsp;Xiaorong Wang ,&nbsp;Yueming Wu ,&nbsp;Kaiguo Xia ,&nbsp;Xiangyu Mu ,&nbsp;Qiang Xuan ,&nbsp;Jun Xiao ,&nbsp;Yaohui He ,&nbsp;Wen Liu ,&nbsp;Xiaoyuan Song ,&nbsp;Fei Sun","doi":"10.1016/j.ncrna.2025.02.002","DOIUrl":"10.1016/j.ncrna.2025.02.002","url":null,"abstract":"","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"12 ","pages":"Pages 65-66"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143548728","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":"PD-L1 pfeRNAs as blood-based predictors of treatment response of unresectable malignant pleural mesothelioma patients administered Durvalumab with cisplatin and pemetrexed as first-line therapy","authors":"Andrei Gurau ,&nbsp;Suguru Yamauchi ,&nbsp;Kaitlyn Ecoff ,&nbsp;Kristen P. Rodgers ,&nbsp;James R. Eshleman ,&nbsp;Charles Conover Talbot Jr ,&nbsp;Peng Huang ,&nbsp;Joshua Choi ,&nbsp;Patrick M. Forde ,&nbsp;Valsamo Anagnostou ,&nbsp;Malcolm Brock ,&nbsp;Yuping Mei","doi":"10.1016/j.ncrna.2025.02.003","DOIUrl":"10.1016/j.ncrna.2025.02.003","url":null,"abstract":"<div><h3>Background</h3><div>A new therapeutic avenue combining Durvalumab with cisplatin-pemetrexed (Durva-CP) has delivered a promising outcome for previously untreated patients with unresectable malignant pleural mesothelioma (MPM) in clinical trials. However, the limited patient response to Durva-CP needs predictors to select optimal candidates and monitor the developed resistance. Protein functional effector sncRNA (pfeRNA) reveals a fundamental mechanism underlying the regulation of protein activity. The common mechanisms underlying durvalumab, cisplatin, and pemetrexed indicate that PD-L1 pfeRNAs (PDLpfeRNAs) are key molecules that control the treatment response.</div></div><div><h3>Methods</h3><div>We specified PDLpfeRNAs by sncRNA deep sequencing, confirmed their binding to PD-L1 by immunoprecipitation and reverse pull-down assays, and demonstrated their roles in controlling the interaction behaviors of PD1/L1 through quality-controlled drug development assays. Following the standards required for the CLIA-compliant LDT, we measured their expression levels in 60 plasma biospecimens from 30 unresectable MPM patients enrolled in the PrE0505 Phase II multicenter study. Using the Cox proportional hazards model and Kaplan-Meier analyses, we described their significance in predicting the treatment response of unresectable MPM patients administered Durva-CP as first-line therapy.</div></div><div><h3>Results</h3><div>Two PDLpfeRNAs, PDLpfeRNAa and PDLpfeRNAb, were characterized, confirmed to bind to PD-L1, and identified to control the interaction behaviors of PD-1/L1. Their plasma relative expression levels (REL) demonstrated significant prognostic value for both overall survival (p = 0.0019) and progression-free survival (p = 0.019), and the association remained significant after adjusting for histological subtype (HR 2.59, 95 % CI: 1.00–6.70, p = 0.050) and age (HR 1.03, 95 % CI: 0.98–1.07, p = 0.269).</div></div><div><h3>Conclusions</h3><div>Plasma PDLpfeRNAs are predictors of treatment response of unresectable MPM patients treated with Durva-CP as first-line therapy to select optimal candidates and monitor the developed resistance.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"12 ","pages":"Pages 34-41"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143509655","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":"Extracellular vesicles derived microRNAs as non-invasive markers of liver fibrosis in chronically infected HCV patients: a pilot study","authors":"Victoria Cairoli ,&nbsp;Daniel Valle-Millares ,&nbsp;Pablo Ryan ,&nbsp;Lourdes Dominguez ,&nbsp;Luz Martín-Carbonero ,&nbsp;Ignacio De los Santos ,&nbsp;Elena De Matteo ,&nbsp;Beatriz Ameigeiras ,&nbsp;Marcela De Sousa ,&nbsp;Verónica Briz ,&nbsp;María V. Preciado ,&nbsp;Amanda Fernández-Rodriguez ,&nbsp;Pamela Valva","doi":"10.1016/j.ncrna.2025.03.004","DOIUrl":"10.1016/j.ncrna.2025.03.004","url":null,"abstract":"&lt;div&gt;&lt;div&gt;Extracellular vesicles (EVs) are an increasingly promising tool for liquid biopsy in liver diseases. Hepatitis C Virus (HCV) infection, alone or together with Human Immunodeficiency Virus (HIV) infection significantly impacts on the microRNA (miRNA) EVs content resembling chronic hepatitis C (CHC) progression. The objective of the study was to delve into the intricate EVs-miRNA profiles in CHC patients with different liver fibrosis stages, aiming to pinpoint non-invasive markers capable of distinguishing significant fibrosis.&lt;/div&gt;&lt;div&gt;Plasma EV-miRNAs from 50 CHC patients (HCV+ and HCV+/HIV+) stratified in no significant (F &lt; 2) and significant (F ≥ 2) fibrosis, were massively sequenced. General linear models (GLM) were used to identify significantly differential expressed (SDE) miRNAs according to liver fibrosis stages (F ≥ 2 and F &lt; 2). Dysregulated biological pathways were subsequently analyzed &lt;em&gt;in silico&lt;/em&gt; for the following groups: i) all patients; ii) HCV+; and iii) HCV+/HIV+. Multiple-ordered logistic regression analysis was performed to develop a score to identify F ≥ 2 cases. The diagnostic potential of both the SDE miRNAs and the developed score was assessed using ROC curve analysis.&lt;/div&gt;&lt;div&gt;With respect to all CHC patients, two SDE miRNAs (hsa-miR-122-5p and hsa-miR-92a-3p) were identified which regulate genes related to cytoskeleton organization. Regarding their diagnostic performance to discriminate F ≥ 2, both miRNAs individually demonstrated acceptable diagnostic values. However, their combined use in a new score enhanced their diagnostic performance (AUROC = 0.833).&lt;/div&gt;&lt;div&gt;In the HCV+ subgroup, 8 SDE miRNAs (hsa-miR-122-5p, hsa-miR-320c, hsa-miR-3615, hsa-miR-320a-3p, hsa-miR-374b-5p, hsa-let-7a-3p, hsa-miR-199a-5p, hsa-miR-142-5p), which regulate macrophage activity and cell growth/death regulation, were recognized. Among them, hsa-miR-3615 displayed the highest diagnostic performance to discriminate F ≥ 2 (AUROC = 0.936).&lt;/div&gt;&lt;div&gt;With respect to HCV+/HIV+, 18 SDE miRNAs (hsa-miR-4508, hsa-miR-122-5p, hsa-miR-451a, hsa-miR-1290, hsa-miR-1246, hsa-miR-107, hsa-miR-15b-5p, hsa-miR-194-5p, hsa-miR-22-5p, hsa-miR-20b-5p, hsa-miR-142-5p, hsa-miR-328-3p, hsa-miR-335-3p, hsa-miR-125a-5p, hsa-miR-423-3p, hsa-let-7d-3p, hsa-miR-128-3p, hsa-miR-10a-5p) were recognized that regulate RNA silencing processes. In this case, hsa-miR-423-3p and hsa-miR-128-3p showed outstanding diagnostic performances (AUROC &gt; 0.900).&lt;/div&gt;&lt;div&gt;Distinct EVs-miRNA profiles were identified in patients with varying liver fibrosis stages, both in the overall CHC cohort and within HCV+ and HCV+/HIV+ subgroups. These specific miRNA signatures would allow the elucidation of potential mechanisms involved in clinical evolution and identification of specific biomarkers of unfavorable progression, plausible to be used in a diagnostic panel. Furthermore, the developed score demonstrates the ability to discriminate within the CHC group those i","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"12 ","pages":"Pages 132-140"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143643439","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":"MiR-326: Role and significance in brain cancers","authors":"Zaira Spinello ,&nbsp;Zein Mersini Besharat ,&nbsp;Fabrizio Mainiero ,&nbsp;Aurelia Rughetti ,&nbsp;Laura Masuelli ,&nbsp;Elisabetta Ferretti ,&nbsp;Giuseppina Catanzaro","doi":"10.1016/j.ncrna.2025.02.006","DOIUrl":"10.1016/j.ncrna.2025.02.006","url":null,"abstract":"<div><div>MicroRNAs (miRNAs) are small non-coding RNAs that act as critical regulators of gene expression by repressing mRNA translation. The role of miRNAs in cell physiology spans from cell cycle control to cell proliferation and differentiation, both during development and in adult tissues. Accordingly, dysregulated expression of miRNAs has been reported in several diseases, including cancer, where miRNAs can act as oncogenes or oncosuppressors. Of note, miRNA signatures are also under investigation for classification, diagnosis, and prognosis of cancer patients.</div><div>Brain tumours are primarily associated with poor prognosis and high mortality, highlighting an urgent need for novel diagnostic, prognostic, and therapeutic tools. Among miRNAs investigated in brain tumours, miR-326 has been shown to act as a tumour suppressor in adult and paediatric brain cancers. In this review, we describe the role of miR-326 in malignant as well as benign cancers originating from brain tissue. In addition, since miR-326 expression can be regulated by other non-coding RNA species, adding a further layer of regulation in the cancer-promoting axis, we discuss this miRNA's role in targeted therapy for brain cancers.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"12 ","pages":"Pages 56-64"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143528734","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":"LncRNA APTR amplification serves as a potential glioma biomarker and promotes glioma progression via miR-6734-5p/ TCF7/LEF1 axis","authors":"Heng Chen ,&nbsp;Mengzhen Huang ,&nbsp;Jiayi Li ,&nbsp;Shanshan Zhang ,&nbsp;Cuiyun Sun ,&nbsp;Wenjun Luo ,&nbsp;Lin Yu","doi":"10.1016/j.ncrna.2025.02.007","DOIUrl":"10.1016/j.ncrna.2025.02.007","url":null,"abstract":"<div><h3>Background</h3><div>Alu-mediated p21 transcriptional regulator (<em>APTR</em>) overexpression is detected in different human cancers; however, few reports have investigated <em>APTR</em> gene amplification conditions. Furthermore, whether <em>APTR</em> amplification is related to glioma malignancy and the underlying mechanism remain unknown.</div></div><div><h3>Methods</h3><div><em>APTR</em> amplification and expression levels in 153 glioma samples were analyzed using qPCR. Correlations between APTR and patient prognosis were evaluated using Kaplan-Meier survival and COX regression analyses. Both <em>in vitro</em> and <em>in vivo</em> phenotypic assays were performed to confirm the carcinogenic effects of APTR in glioblastoma (GBM) cells. RNA-sequencing and RNA immunoprecipitation and luciferase reporter assays were performed to confirm APTR as a competing endogenous RNA (ceRNA) and to identify the downstream axis of APTR.</div></div><div><h3>Results</h3><div>Our results suggest that <em>APTR</em> amplification and overexpression are novel independent diagnostic biomarkers for predicting poor prognosis in patients with gliomas. APTR knockdown significantly repressed the proliferation and invasion of GBM cells, both <em>in vitro</em> and <em>in vivo</em>. APTR was demonstrated to absorb miR-6734-5p and upregulate TCF7 and LEF1 expression. Taken together, these results suggest that APTR promotes the malignant phenotypes of GBM by inducing TCF7 and LEF1 expression.</div></div><div><h3>Conclusion</h3><div>We identified APTR as a novel prognostic biomarker in patients with gliomas and confirmed that APTR is a ceRNA that promotes glioma progression via the APTR/miR-6734-5p/TCF7/LEF1 axis.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"12 ","pages":"Pages 42-55"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143520611","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":"2025-06-01","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":"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":"2025-04-01","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}