Non-coding RNA Research最新文献

{"title":"Long non-coding RNAs in B-cell acute lymphoblastic leukemia: Disease implication, challenges and therapeutic opportunities","authors":"Devesh Srivastava,&nbsp;Ashish Misra","doi":"10.1016/j.ncrna.2025.09.005","DOIUrl":"10.1016/j.ncrna.2025.09.005","url":null,"abstract":"<div><div>B-cell acute lymphoblastic leukemia (B-ALL) manifests as an abnormal proliferation of neoplastic B-cell lymphocytes, adversely affecting both children and adults. Despite the advancements in cancer research, B-ALL cure remains challenging due to the complexity of the disease and immense subtype heterogeneity. Better understanding of the molecular mechanisms driving B-ALL pathogenesis is imperative to identify the novel therapeutic markers that can impede disease progression. Genomic and transcriptomic studies involving patient samples have underscored the emerging role of long non-coding RNAs (lncRNAs) in the diverse B-ALL landscape. Their dysregulation has been linked to malignant proliferation, metastasis, and varying patient survival outcomes. Gaining detailed mechanistic insights into the role of lncRNAs in B-ALL pathophysiology is pivotal for understanding their contributions to disease progression and developing new therapeutics. Herein, we have comprehensively discussed B-ALL and its diverse subtypes, focusing on the pivotal role played by various lncRNAs in fine-tuning signaling pathways, disease heterogeneity and progression. We have also explored recent advances in our understanding of the diverse classes of lncRNA inhibitors, evaluating their potential as B-ALL therapeutics and challenges associated with their development.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"16 ","pages":"Pages 40-56"},"PeriodicalIF":4.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145223226","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":"Keratinocyte-specific long non-coding RNA NR037661 controls alternative splicing of ANGPTL4 to induce keratinocyte differentiation","authors":"Chunxiao Li ,&nbsp;Qinyuan Zhu ,&nbsp;Xinhang Cao ,&nbsp;Dandan Xiao ,&nbsp;Hui Yang ,&nbsp;Xiang Kong ,&nbsp;Ziyu Wang ,&nbsp;Mingzhe Ma ,&nbsp;Yangbai Sun","doi":"10.1016/j.ncrna.2025.10.003","DOIUrl":"10.1016/j.ncrna.2025.10.003","url":null,"abstract":"<div><h3>Background</h3><div>Aberrant differentiation of keratinocytes has been implicated in various skin diseases. However, the impact of lncRNA on keratinocyte differentiation and RNA alternative splicing remains poorly understood. The primary aim of this study was to delineate the landscape of differentially expressed lncRNAs in keratinocytes undergoing differentiation and to elucidate the underlying molecular mechanisms.</div></div><div><h3>Methods</h3><div>Primary human keratinocytes (HKEn) were subjected to comprehensive microarray analysis to identify the differentially expressed lncRNAs upon calcium stimulation. Loss-of-function experiments were carried out to explore the role of NR037661 in keratinocyte differentiation. RNA sequencing analysis was performed to study the potential target genes of NR037761. RNA pull-down assay, SDS-PAGE, silver staining and mass spectrometry analysis were utilized to explore the potential proteins that interacted with NR037761 and participated in NR037761-mediated keratinocyte differentiation. The effects of NR037761 on the alternative splicing and expression of Angiopoietin-like 4 (ANGPTL4) were analyzed by RT-PCR and Western blot.</div></div><div><h3>Results</h3><div>NR037661 specifically interacts with the splicing factor Serine/arginine repetitive matrix protein 2 (SRRM2), facilitating its nuclear localization. This interaction modulates the alternative splicing (AS) of ANGPTL4 mRNA, ultimately influencing keratinocyte differentiation.</div></div><div><h3>Conclusions</h3><div>Our findings illuminate a novel regulatory mechanism underlying keratinocyte differentiation, potentially revealing new therapeutic targets for skin diseases.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"16 ","pages":"Pages 93-103"},"PeriodicalIF":4.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145418116","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":"AQUARIUM_HB: a bioinformatics pipeline for human blood circular RNA analysis","authors":"Shaoxun Yuan ,&nbsp;Xue Bai ,&nbsp;Linwei Li ,&nbsp;Wanjun Gu","doi":"10.1016/j.ncrna.2025.09.004","DOIUrl":"10.1016/j.ncrna.2025.09.004","url":null,"abstract":"<div><div>Accurately identifying and quantifying human blood circular RNAs (circRNAs) from RNA-seq data is a critical bioinformatics challenge in biomarker discovery for human diseases. In this study, we present <em>AQUARIUM-HB</em>, a comprehensive bioinformatics pipeline for identifying, quantifying, annotating, and analyzing circRNAs from human blood transcriptomes. <em>AQUARIUM-HB</em> includes three functional modules. First, it identifies and annotates circRNAs from rRNA-depleted RNA-seq datasets of human blood samples. Second, it performs an in-depth expression analysis of blood circRNAs. Third, it constructs a reference set of full-length blood circRNAs. We demonstrate the application of <em>AQUARIUM-HB</em> using a human blood RNA-seq dataset from COVID-19 patients, showcasing its potential for improving the accuracy and depth of circRNA biomarker discovery.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"16 ","pages":"Pages 32-39"},"PeriodicalIF":4.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145159901","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":"Illustration of the variable 1D sequences but conserved 2D and 3D structures of different ncRNA nanostructures for tracking the evolution and origin of organisms","authors":"Kai Jin ,&nbsp;Margaret Bohmer ,&nbsp;Peixuan Guo","doi":"10.1016/j.ncrna.2025.09.003","DOIUrl":"10.1016/j.ncrna.2025.09.003","url":null,"abstract":"<div><div>Viruses and other microorganisms are constantly mutating and emerging in different regions. Here, we apply nanotechnology to examine the primary, secondary, and tertiary structures of novel noncoding RNA nanoparticles and find that primary sequences (1D) vary widely between viruses, while secondary (2D) and tertiary structures (3D) are highly conserved. The uniqueness of the phi29 system makes this reported study possible. RNA evolution studies are relevant to the concept of RNA as the origin of life. The recent discovery that RNA is a motile and recombinant entity supports the hypothesis that RNA is the substance of life. Previously, we reported noncoding RNA nanoparticles packaging RNA (pRNA) of the Bacillus virus phi29 (Nature Nanotechnology, 2011, PMID: 21909084; Nature Nanotechnology, 2010, PMID: 21102465; Science, 1987, PMID: 3107124). Phi29 can infect spore-forming Bacillus subtilis, which has long been hidden in the soil with slow or no evolution due to the protection of spores. They are living fossils. The pRNA of the phi29 DNA packaging motor drives the viral motor for DNA transport. In this study, we used existing datasets to search for more pRNAs. Their primary sequence diversity makes it challenging to identify them from the whole genomes of other species. Using the top-down (1D) approach and the bottom-up assembly (3D) approaches, we found that their 2D and 3D structures are highly conserved. Structural conservation enabled us to apply the two-dimensional structure-based approach to find these ncRNAs from databases and identify 12 new pRNAs. The presence of two additional components in the genome, a motor channel protein and a motor ATPase, further confirmed the authenticity of these pRNAs and supported the conclusion that these pRNAs are motor-driven components. Highly conserved and paired left and right loops for assembling the pRNA hexamer were identified in all 12 pRNAs. Artificial modification of the pairing and determination of the virion production activity of the mutated phi29 pRNA further confirmed the conclusion that the secondary and tertiary structures are highly conserved. Understanding the retention, conservation, and variation of viral non-coding RNA sequences and structure can help us trace the evolutionary history of the virus, find lineage information, and provide important information about the origin of the viruses. It can also provide knowledge for the design of disease prevention and treatment by providing the background for <em>in vivo</em> RNA nanotechnology.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"16 ","pages":"Pages 156-166"},"PeriodicalIF":4.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145568724","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":"List of reviewers in 2025","authors":"","doi":"10.1016/j.ncrna.2026.01.005","DOIUrl":"10.1016/j.ncrna.2026.01.005","url":null,"abstract":"","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"16 ","pages":"Pages 178-180"},"PeriodicalIF":4.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022445","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":"Non-coding RNAs in congenital heart disease and placental development: Bridging molecular mechanisms to clinical biomarkers and therapies","authors":"Haoxuan Wang ,&nbsp;Xinzhe Chen ,&nbsp;Yinghui Li ,&nbsp;Shudan Xiao ,&nbsp;Tianqi Teng ,&nbsp;Sumin Yang ,&nbsp;Kun Wang ,&nbsp;Meihua Zhang","doi":"10.1016/j.ncrna.2025.08.006","DOIUrl":"10.1016/j.ncrna.2025.08.006","url":null,"abstract":"<div><div>Non-coding RNAs (ncRNAs) have emerged as pivotal regulators of gene expression, orchestrating embryonic development and disease pathogenesis. This review synthesizes current knowledge on the origin, biogenesis, and functional diversity of ncRNAs, with a focus on their regulatory crosstalk in congenital heart disease (CHD) and placental development. The fetal heart-placenta axis, a bidirectional signaling network essential for cardiogenesis and placental morphogenesis, is spatiotemporally modulated by ncRNAs through epigenetic and post-transcriptional mechanisms. Through precise regulation of cardiac cell differentiation, angiogenesis, and trophoblast invasion, ncRNAs maintain developmental homeostasis, whereas their dysregulation disrupts these processes, contributing to CHD pathogenesis and positioning them as promising biomarkers. Collectively, this review establishes ncRNAs as molecular bridges between the fetal heart-placenta axis and clinical translation, underscoring their dual utility as diagnostic biomarkers for CHD and modifiable targets to correct placental maldevelopment, thereby advancing precision therapies for congenital disorders.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"16 ","pages":"Pages 1-20"},"PeriodicalIF":4.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145159899","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-EME1 enhances BRCA1 recruitment and alters repair of DNA damage in cervical cancer radioresistance","authors":"Qing Li,&nbsp;Zhenyu Zhou,&nbsp;Xiaoying Li,&nbsp;Qiongyu Lan","doi":"10.1016/j.ncrna.2025.09.006","DOIUrl":"10.1016/j.ncrna.2025.09.006","url":null,"abstract":"<div><h3>Background</h3><div>Cervical cancer is a significant cause of mortality in women globally, and radioresistance limits the effectiveness of standard radiotherapy treatment. Exploring the molecular mechanisms that contribute to radioresistance is vital for improving therapies. This study focuses on the role of lncRNA in influencing the radioresistance of cervical cancer.</div></div><div><h3>Methods</h3><div>We identified lncRNA-EME1 as a candidate regulator of cervical cancer radioresistance through transcriptomic sequencing and RT-qPCR. Its function was explored by silencing or overexpressing lncRNA-EME1, followed by proliferation (MTT), clonogenic survival, apoptosis, and ROS assays. Effects on BRCA1 expression and DNA damage response were examined by WB, γ-H2AX focus analysis, and the I-SceI-mediated homologous recombination assay. Mechanistic insights were obtained using RNA pull-down and RIP assays. Finally, a xenograft model with subsequent TUNEL and immunohistochemical analyses was used to validate the role of lncRNA-EME1 in regulating BRCA1 and mediating radioresistance <em>in vivo</em>.</div></div><div><h3>Results</h3><div>Our findings indicate that lncRNA-EME1 is overexpressed in radioresistant cervical cancer cells. Silencing lncRNA-EME1 enhances radiosensitivity in HeLa-IR and SiHa-IR cells, suppresses malignant phenotypes, and increases apoptosis and ROS levels. This effects corresponds with reduced BRCA1 expression and alterations in DNA damage repair markers, highlighting its role in the radiation response. The positive association between lncRNA-EME1 and BRCA1 further supports its involvement in DNA damage repair, thereby regulating cervical cancer cells' sensitivity to radiation therapy. <em>In vivo</em> xenograft experiments further confirmed that lncRNA-EME1 promotes BRCA1 expression and contributes to cervical cancer radioresistance.</div></div><div><h3>Conclusion</h3><div>This study sheds light on the role of lncRNA-EME1 in regulating BRCA1 activity and contributing to cervical cancer radioresistance. Our data reveals that decreasing lncRNA-EME1 expression could potentially boost radiosensitivity in cervical cancer cells.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"16 ","pages":"Pages 57-69"},"PeriodicalIF":4.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145223225","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":"Integrative analysis of tissue and circulating miRNAs as biomarkers for progression and survival in hepatocellular carcinoma","authors":"Abdullah Jabri ,&nbsp;Abdulaziz Mhannayeh ,&nbsp;Mohamed Alsharif ,&nbsp;Bader Taftafa ,&nbsp;Tooba Mujtaba ,&nbsp;Arshiya Akbar ,&nbsp;Ahmed Abu-zaid ,&nbsp;Tanveer Ahmad Mir ,&nbsp;Mohammad Imran Khan ,&nbsp;Firoz Ahmed ,&nbsp;Itika Arora ,&nbsp;Ahmed Yaqinuddin","doi":"10.1016/j.ncrna.2025.11.002","DOIUrl":"10.1016/j.ncrna.2025.11.002","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality, with limited biomarkers available for early diagnosis and risk stratification. In this study, we performed an integrative analysis of tissue and circulating microRNA (miRNA) expression profiles to identify candidates linked to disease progression and clinical outcomes. Tumor miRNA data from The Cancer Genome Atlas Liver Hepatocellular Carcinoma (TCGA-LIHC) and serum miRNA data from the Gene Expression Omnibus (GSE113740) were analyzed using differential expression, survival analysis, functional enrichment, and clinical subgroup evaluation. We identified 16 significantly dysregulated miRNAs in HCC tissues, including hsa-miR-187 and hsa-miR-6718, which were associated with poor survival, and hsa-miR-5589, which showed a protective effect. Clinical analyses revealed stage-specific upregulation of hsa-miR-106b and downregulation of the hsa-miR-124 family in metastatic tumors. Functional enrichment highlighted pathways such as PI3K-Akt, MAPK signalling, and nucleocytoplasmic transport. Circulating miRNAs, including hsa-miR-3619-3p, hsa-miR-1290, and hsa-miR-1185-2-3p, correlated with AFP levels and disease stage, underscoring their value as non-invasive biomarkers. These findings demonstrate that integrated analysis of tissue and serum miRNAs can identify clinically relevant biomarkers and potential therapeutic targets in HCC.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"16 ","pages":"Pages 167-177"},"PeriodicalIF":4.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145614881","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":"miR-6850 drives phenotypic changes and signaling in high grade serous ovarian cancer","authors":"Kamil Filipek ,&nbsp;Daniela Pollutri ,&nbsp;Ivana Kurelac ,&nbsp;Giuseppe Gasparre ,&nbsp;Marianna Penzo","doi":"10.1016/j.ncrna.2025.10.004","DOIUrl":"10.1016/j.ncrna.2025.10.004","url":null,"abstract":"<div><div>MicroRNAs (miRNAs) are key post-transcriptional regulators of gene expression, and their dysregulation is closely linked to cancer development. Ovarian cancer (OC), particularly the high-grade serous ovarian carcinoma (HGSOC) subtype, is the most lethal gynecological malignancy, primarily due to late-stage diagnosis and limited treatment options. Among the miRNAs encoded at the often amplified 8q24.3 region, miR-6850 has emerged as a potential candidate target owing to its genomic positioning inside this hotspot and its unexpectedly low expression in HGSOC tissues and cell lines. In silico investigations indicated that, despite the gain in MIR6850 copy number, its mature products, miR-6850-5p and miR-6850-3p, were expressed at low levels; notably, <em>MIR6850</em> gene amplification was associated with enhanced disease-specific survival. Functional studies revealed that ectopic production of both isoforms in SKOV-3 and NIH:OVCAR3 cells inhibited proliferation, compromised clonogenic capacity, and disturbed cell cycle progression. Moreover, miR-6850 altered cell phenotype by facilitating mesenchymal-to-epithelial transition (MET), as shown by the overexpression of E-cadherin and β-catenin and the downregulation of Slug and Vimentin. It also regulated cell adhesion and migration while reducing global protein synthesis via the downregulation of the PI3K/Akt/mTOR pathway. Our results together identify miR-6850 as a tumor-suppressive miRNA in HGSOC, demonstrating its diverse anti-oncogenic actions and underscoring its potential as a prognostic biomarker and therapeutic target in ovarian cancer.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"16 ","pages":"Pages 104-116"},"PeriodicalIF":4.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145466251","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":"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":"2025-12-01","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}