Non-coding RNA Research最新文献

{"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}

{"title":"LncRNA MIR155HG suppresses cell apoptosis by activating autophagy via miR-7036b-3p/GPNMB axis and AMPK/mTOR signaling in spinal cord injury","authors":"Ruoxi Liu ,&nbsp;Jintao Ye ,&nbsp;Sihua Huang","doi":"10.1016/j.ncrna.2025.05.013","DOIUrl":"10.1016/j.ncrna.2025.05.013","url":null,"abstract":"<div><h3>Background</h3><div>Long non-coding RNAs (lncRNAs) participate in spinal cord injury (SCI) development through regulating autophagy and neuronal apoptosis. Previously, <em>MIR155HG</em> was identified as an upregulated lncRNA in rat bladder tissues harvested after SCI operation. Our study aimed to elucidate the function of <em>MIR155HG</em> in SCI.</div></div><div><h3>Methods</h3><div>Glutamate (Glu)-stimulated primary mouse spinal cord neurons were used as SCI cellular models. Contusion-induced SCI mouse models were established using an improved weightlessness method. Neuronal apoptosis and autophagy affected by <em>MIR155HG</em> or <em>GPNMB</em> silencing were assessed by TUNEL staining, flow cytometry assay, western blotting, and immunofluorescence staining. The binding of miR-7036b-3p on <em>MIR155HG</em> (or <em>GPNMB</em>) was verified by luciferase reporter assay. Histological changes were observed through HE and Masson staining.</div></div><div><h3>Results</h3><div><em>MIR155HG</em> and <em>GPNMB</em> expression was elevated while miR-7036b-3p expression was reduced in SCI. <em>MIR155HG</em> silencing attenuated the apoptosis in Glu-stimulated neurons and ameliorated glial scar formation and motor function of SCI mice. <em>GPNMB</em> knockdown mitigated apoptosis, enhanced autophagy, activated AMPK phosphorylation, and repressed mTOR phosphorylation. <em>MIR155HG</em> upregulated <em>GPNMB</em> expression by sponging miR-7036b-3p. The autophagy inhibitor 3-MA reversed the above changes caused by <em>GPNMB</em> depletion.</div></div><div><h3>Conclusion</h3><div><em>MIR155HG</em> knockdown alleviated neuronal apoptosis by enhancing autophagy in SCI via miR-7036b-3p/<em>GPNMB</em> axis and AMPK/mTOR pathway.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"15 ","pages":"Pages 1-17"},"PeriodicalIF":5.9,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144623537","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-92a-1-5p contributes to cellular proliferation and survival in chronic myeloid leukemia and its inhibition enhances imatinib efficacy","authors":"Joanne Peters ,&nbsp;Emeline Bollaert ,&nbsp;Anne-Sophie Cloos ,&nbsp;Melissa Claus ,&nbsp;Ahmed Essaghir ,&nbsp;Sandrine Lenglez ,&nbsp;Pascale Saussoy ,&nbsp;Guillaume Dachy ,&nbsp;Pierre Autin ,&nbsp;Jean-Baptiste Demoulin ,&nbsp;Violaine Havelange","doi":"10.1016/j.ncrna.2025.05.008","DOIUrl":"10.1016/j.ncrna.2025.05.008","url":null,"abstract":"<div><div>Tyrosine kinase inhibitors (TKI), such as imatinib, have revolutionized chronic myeloid leukemia (CML) treatment. Despite this success, TKI intolerance and resistance remain significant clinical challenges. A promising therapeutic approach is to simultaneously target the <em>BCR::ABL1</em> oncogene and other oncogenic drivers. The polycistronic <em>miR-17-92</em> cluster is known to contribute to CML development and progression, but the specific roles of <em>miR-92a-1-5p</em> within this cluster remain unclear. In this study, we assess the roles of this microRNA and evaluate the therapeutic potential of combining microRNA inhibition with imatinib to improve treatment outcome. Our results show that <em>miR-92a-1-5p</em> is downregulated by imatinib in myeloid cell lines harboring <em>BCR::ABL1</em> and in CML patient samples. Inhibition of <em>miR-92a-1-5p</em> reduces proliferation and enhances imatinib-induced cell death, while its overexpression increases proliferation and counteracts the effects of imatinib on cell death. This decrease in proliferation caused by <em>miR-92a-1-5p</em> inhibition is rescued after simultaneous inhibition of two newly identified target genes: <em>BNIP3L (NIX)</em> and <em>TP53INP1</em>. We confirm that <em>miR-92a-1-5p</em> regulates proliferation and cell cycle by targeting <em>TP53INP1</em> and decreases autophagy by targeting <em>BNIP3L</em>. Our data suggest that <em>miR-92a-1-5p</em> plays a role in CML progression, and its inhibition enhances imatinib anti-leukemic efficacy, making it a potential therapeutic target.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"14 ","pages":"Pages 14-24"},"PeriodicalIF":5.9,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144203874","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":"Computational discovery of conserved RNA structures and functional characterization of a structured lncRNA in Leishmania braziliensis","authors":"Caroline R. Espada ,&nbsp;Christian Anthon ,&nbsp;Rubens D.M. Magalhães ,&nbsp;José Carlos Quilles Junior ,&nbsp;Natalia M.M. Teles ,&nbsp;Fabiano S. Pais ,&nbsp;Lissur A. Orsine ,&nbsp;Letícia de Almeida ,&nbsp;Tânia P.A. Defina ,&nbsp;Adam Dowle ,&nbsp;Jan Gorodkin ,&nbsp;Pegine B. Walrad ,&nbsp;Angela K. Cruz","doi":"10.1016/j.ncrna.2025.05.010","DOIUrl":"10.1016/j.ncrna.2025.05.010","url":null,"abstract":"<div><div><em>Leishmania</em> parasites alternate between hosts, facing environmental changes that demand rapid gene expression adaptation. Lacking canonical RNA polymerase II promoters, transcription in these eukaryotes is polycistronic, with gene regulation occurring post-transcriptionally. Although non-coding RNAs (ncRNAs) have been identified in <em>Leishmania</em> transcriptomes, their functions remain unclear. Recognizing RNA structure's importance, we performed a genome-wide alignment of <em>L. braziliensis</em> and related species, identifying conserved RNA structures, 38 of which overlap with known ncRNAs. One such ncRNA, <em>lncRNA45</em>, was functionally characterized. Using a knockout cell line, we demonstrated that <em>lncRNA45</em> is crucial for parasite fitness. Reintroducing the wild type <em>lncRNA45</em> restored fitness, while a version with a single nucleotide substitution in the structured region did not. This mutation also altered RNA-protein interactions. These findings suggest that <em>lncRNA45</em>'s regulatory role and protein interactions rely on its secondary structure. This study highlights the significance of structured lncRNAs in <em>Leishmania</em> biology and their potential as therapeutic targets. Further research into these ncRNAs could uncover new parasite regulation mechanisms and inspire novel treatment strategies.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"14 ","pages":"Pages 51-64"},"PeriodicalIF":5.9,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144220902","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":"Exosome-derived hsa_circ_0007132 promotes lenvatinib resistance by inhibiting the ubiquitin-mediated degradation of NONO","authors":"Mingbo Cao ,&nbsp;Yuxuan Li ,&nbsp;Xiaorui Su ,&nbsp;Yongchang Tang ,&nbsp;Feng Yuan ,&nbsp;Yupeng Ren ,&nbsp;Meihai Deng ,&nbsp;Zhicheng Yao","doi":"10.1016/j.ncrna.2025.05.007","DOIUrl":"10.1016/j.ncrna.2025.05.007","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) is a highly heterogeneous solid tumor, with its incidence showing a troubling upward trend over the past decade. Lenvatinib is one of the first-line medications for treating advanced HCC, however, the development of resistance significantly undermines its potential to improve patient prognosis. In recent years, exosomal circRNAs have been implicated in the resistance mechanisms of various cancers, yet their role in mediating lenvatinib resistance (LR) remains largely unexplored. In this study, we identified hsa_circ_0007132, which is upregulated in the serum exosomes of HCC patients exhibiting progressive disease (PD) following lenvatinib treatment. Subsequently, we employed LR cell lines to conduct both <em>in vitro</em> and <em>in vivo</em> experiments, which provided compelling evidence that hsa_circ_0007132 significantly promotes LR in HCC. Mechanistically, hsa_circ_0007132 interacts with the NONO protein, impairing its ubiquitination and leading to increased stability and upregulation of NONO expression, thereby enhancing NONO-mediated nuclear export of ZEB1 mRNA and elevating ZEB1 protein expression, which ultimately contributes to LR. In summary, our findings unveil a critical mechanism through which HCC mediates tumor progression and LR via exosomal hsa_circ_0007132, while also emphasizing that targeting NONO may represent a promising therapeutic strategy to overcome LR.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"14 ","pages":"Pages 1-13"},"PeriodicalIF":5.9,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144169787","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":"Role of Ocrelizumab in modulating gene and microRNA expression in multiple sclerosis","authors":"Bruna De Felice ,&nbsp;Elisabetta Signoriello ,&nbsp;Concetta Montanino ,&nbsp;Giuseppe Romano ,&nbsp;Deborah Archetto ,&nbsp;Elisabetta Maida ,&nbsp;Martina Marciano ,&nbsp;Simona Bonavita ,&nbsp;Giacomo Lus ,&nbsp;Federica Farinella ,&nbsp;Cinzia Coppola","doi":"10.1016/j.ncrna.2025.05.009","DOIUrl":"10.1016/j.ncrna.2025.05.009","url":null,"abstract":"<div><div>Multiple sclerosis is an autoimmune neurodegenerative disease and one of the most significant challenges in modern neurology, impacting approximately 2.8 million people globally. As a multifactorial condition, susceptibility to MS can result from a combination of genetic and environmental factors. Current treatment strategies aim to prevent acute attacks, slow disease progression, and alleviate symptoms. Ocrelizumab, a monoclonal antibody targeting CD20, has demonstrated efficacy in clinical trials by reducing both disease activity and frequency of relapses.</div><div>Given the recent approval of this treatment, we investigated whether Ocrelizumab alters the expression of key miRNAs and genes involved in neuroinflammation, such as let-7a-5p, miR-14a-5p, miR-21a-5p, miR-338-3p, IL-1, IL-6, NEAT1, NEFL, NESTIN, SLC16A10 and TNF-alpha, by comparing their expression in patients’ blood before and after one year of treatment with Ocrelizumab. Additionally, we explored potential inverse correlations and direct or indirect interactions among the genes and miRNAs that showed significant changes in expression. Lastly, we conducted a pathway analysis to understand the overall effects potentially exerted by the drug.</div><div>Results revealed a significant decrease in the expression of TNF-alpha, SLC16A10, NEFL and IL-6, and an increase in let-7a-5p expression. There was an inverse correlation between let-7a-5p and the four genes, while the genes positively correlated with each other, suggesting let-7a-5p as a common modulator. These findings indicate that further investigation is needed to determine if the drug directly upregulates let-7a-5p, thereby downregulating the four genes, or if these expression changes are an indication of an overall reduction in inflammation.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"13 ","pages":"Pages 174-183"},"PeriodicalIF":5.9,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144138851","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":"Tongue squamous cell carcinoma-derived exosomes miR-21-5p affect tumor progression via promoting M2 macrophage polarization","authors":"Zixian Xu ,&nbsp;Xin Fang ,&nbsp;Shan Wang ,&nbsp;Jiabei Mu ,&nbsp;Qixian Gai ,&nbsp;Yantong Chen ,&nbsp;Zheyi Sun ,&nbsp;Jiemei Zhai","doi":"10.1016/j.ncrna.2025.05.006","DOIUrl":"10.1016/j.ncrna.2025.05.006","url":null,"abstract":"<div><div>Exosome-mediated intercellular communication plays a key role in shaping the tumor microenvironment and promoting tumor progression. Recent studies have demonstrated that tumor exosomal miRNAs significantly contribute to the polarization of tumor-associated macrophages (TAMs). However, the molecular mechanisms underlying miRNA-mediated regulation of macrophage polarization by exosomes derived from tongue squamous cell carcinoma (TSCC) remain incompletely elucidated. In this study, small RNA sequencing analysis of exosomal miRNAs revealed miR-21-5p was highly expressed in TSCC-derived exosomes. Further investigation demonstrated a significant association between exosomal miR-21-5p and M2 polarization of tumor-associated macrophages (TAMs). Functionally, TSCC-derived exosomes promoted the polarization of M0 macrophages towards the M2 phenotype. Mechanistically, exosomal miR-21-5p enhanced M2 polarization of TAMs by inhibiting phosphorylation of ERK1/2. Additionally, we performed single-sample gene set enrichment analysis (ssGSEA), constructed a multivariate Cox regression model, and performed survival analysis using paired RNA transcriptome and clinical data from TSCC patients. Our results revealed a significant enrichment of M2 macrophages in the tumor microenvironment (TME) of TSCC compared to adjacent normal tissue. Furthermore, we confirmed that M2 macrophages infiltration is associated with poor prognosis in TSCC patients. In summary, our study demonstrates that TSCC-derived exosomal miR-21-5p plays an critical role in M2 macrophage polarization, and M2 macrophages infiltration contributes to the progression of TSCC. Therefore, these findings suggest that therapeutic targeting of miR-21-5p may represent a novel strategy for TSCC treatment by selectively modulating the M2 polarization of TAMs.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"13 ","pages":"Pages 184-196"},"PeriodicalIF":5.9,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144166650","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":"Characterization of small nucleolar RNA retaining transcripts in human normal and cancer cells","authors":"Guglielmo Rambaldelli ,&nbsp;Sidra Asghar ,&nbsp;Giulia Venturi ,&nbsp;Federico Zacchini ,&nbsp;Margherita Serra ,&nbsp;Catia Giovannini ,&nbsp;Laura Gramantieri ,&nbsp;Marco Bernini ,&nbsp;Alberto Inga ,&nbsp;Erik Dassi ,&nbsp;Lorenzo Montanaro","doi":"10.1016/j.ncrna.2025.05.004","DOIUrl":"10.1016/j.ncrna.2025.05.004","url":null,"abstract":"<div><div>Small nucleolar RNAs are non-coding RNAs typically encoded within the introns of both protein-coding and non-coding genes. Interestingly, a significant fraction of snoRNA sequences is found as retained introns of specific mRNA isoforms expressed from their host gene. In the present study, we aimed to define the representation of small nucleolar RNA retaining transcripts across various human cell types and tissues including cancer. We found that these type of transcripts are widely represented in normal tissues and cancer-derived cell lines, appearing both in their full-length form and, frequently, in a shorter variant. We characterized the shortening position, which occurs at or very close to the retained small nucleolar RNA sequence at the 5′ end. Interestingly, for some transcripts this shorter variant represents the only form detected. In addition, some of the small nucleolar RNA retaining transcripts can be localized into the cellular cytoplasmic fraction. Moreover, our findings point out that a variable but consistent proportion of small nucleolar RNA sequences in cells, tissues, and liquid biopsy samples is, in fact, present as small nucleolar RNA retaining transcripts, indicating that these elements should be carefully considered when snoRNA are evaluated as biomarkers. Considering that short reads and gene-based transcriptomic analysis completely overlooked these transcripts, potentially missing critical insights into their involvement in cancer and other diseases, our results strongly indicate that these type of transcripts should be further investigated in different contexts to better understand their biogenesis, sequence features, presence, and role within cells.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"13 ","pages":"Pages 153-161"},"PeriodicalIF":5.9,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144124963","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}