Non-coding RNA Research最新文献

{"title":"Long non-coding RNA AK023617 orchestrates atherosclerosis by regulating the circadian rhythm of immunity-related GTPase family M protein in macrophages","authors":"Rongzhe Lu ,&nbsp;Hengxuan Cai ,&nbsp;Yige Liu ,&nbsp;Guanpeng Ma ,&nbsp;Jiaxin Wang ,&nbsp;Miao Yan ,&nbsp;Zhenming Zhang ,&nbsp;Bo Yu ,&nbsp;Zhaoying Li ,&nbsp;Shaohong Fang","doi":"10.1016/j.ncrna.2024.12.008","DOIUrl":"10.1016/j.ncrna.2024.12.008","url":null,"abstract":"<div><div>Acute coronary events show a diurnal rhythm, and atherosclerotic plaque vulnerability, as a histomorphological characteristic of major adverse cardiovascular events, is a key target for intervention. Although oscillating microRNAs reduce plaque stability by facilitating macrophage apoptosis in lesions, whether rhythmic long non-coding RNA (lncRNA) can regulate diurnal oscillations in plaque stability and the potential underlying mechanism remain unclear. In this study, we examined whether rhythmic lncRNAs are involved in the pathogenesis and progression of atherosclerosis and detected a novel circadian lncRNA-AK023617, which is positively correlated with the peak occurrence of major adverse cardiovascular events. Transfection of short interfering RNA specific to lnc-AK023617 into THP-1 cells dampened the oscillation of immunity-related GTPase family M protein 1 (Irgm1), which is negatively related to plaque stability. In ApoE^−/− mice fed a high-fat diet for 12 weeks, diurnal variations in lncAK023617 were consistent with the proportions of necroptotic cells in atherosclerotic plaques. In addition, reduced expression of lncAK023617 inhibited P-RIP3 and P-MLKL in THP-1 cells. Mechanistically, lncAK023617 interacted with the core molecular clock Bmal1 and promoted nuclear translocation of Bmal1, which could directly bind to the E-BOX elements in the <em>Irgm1</em> promoter. Thus, oscillating lncAK023617 in macrophages can affect plaque stability by regulating necroptosis, which regulates circadian expression of the target gene <em>Irgm1</em> by increasing the transcriptional activity of Bmal1, ultimately determining the diurnal oscillations in plaque stability. Therefore, lncAK023617 may serve as a specific target to ameliorate atherosclerotic plaque vulnerability.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 262-272"},"PeriodicalIF":5.9,"publicationDate":"2024-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11788686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143123785","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":"DNA methylation of long noncoding RNA cytochrome B in diabetic retinopathy","authors":"Renu A. Kowluru,&nbsp;Jay Kumar,&nbsp;Pooja Malaviya","doi":"10.1016/j.ncrna.2024.12.007","DOIUrl":"10.1016/j.ncrna.2024.12.007","url":null,"abstract":"<div><div>Diabetic retinopathy, a microvascular complication of diabetes, is the leading cause of blindness in adults, but the molecular mechanism of its development remains unclear. Retinal mitochondrial DNA is damaged and hypermethylated, and mtDNA-encoded genes are downregulated. Expression of a long noncoding RNA (larger than 200 nucleotides, which does not translate into proteins), encoded by mtDNA, cytochrome B (Lnc<em>CytB</em>), is also downregulated. This study aims to investigate the role of DNA methylation in the downregulation of Lnc<em>CytB</em> in diabetic retinopathy. Human retinal endothelial cells, incubated in 5 mM (normal) or 20 mM (high) D-glucose, in the presence/absence of Azacytidine (a DNA methyl transferase inhibitor) were analyzed for Lnc<em>CytB</em> DNA methylation by immunoprecipitation and methylation specific PCR techniques, and Lnc<em>CytB</em> transcripts by strand-specific PCR and RNA-FISH. Mitochondrial genomic stability was evaluated by quantifying protective mtDNA nucleoids by SYBR green staining and by flow cytometry, and functional stability by oxygen consumption rate using Seahorse analyzer. Results were confirmed in an <em>in vivo</em> model using retina from diabetic rat. While high glucose elevated 5 mC and the ratio of methylated to unmethylated amplicons at Lnc<em>CytB</em> and downregulated its transcripts, azacytidine prevented Lnc<em>CytB</em> DNA hypermethylation and decrease in its expression. Azacytidine also ameliorated decrease in nucleoids and oxygen consumption rate. Similarly, azacytidine prevented increase in retinal Lnc<em>CytB</em> DNA methylation and decrease in its expression in diabetic rats. Thus, DNA hypermethylation plays a major role in the downregulation of retinal Lnc<em>CytB</em> in diabetes, resulting in impaired mitochondrial homeostasis, and culminating in the development of diabetic retinopathy.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 141-149"},"PeriodicalIF":5.9,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142984955","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 transcripts in Mycobacterium tuberculosis-host interactions","authors":"Mahalakshmi Vijayaraghavan ,&nbsp;Shrikanth S. Gadad ,&nbsp;Subramanian Dhandayuthapani","doi":"10.1016/j.ncrna.2024.12.005","DOIUrl":"10.1016/j.ncrna.2024.12.005","url":null,"abstract":"<div><div>Tuberculosis (TB) persists as a significant health threat, affecting millions of people all over the world. Despite years of control measures, the elimination of TB has become a difficult task as morbidity and mortality rates remain unaffected for several years. Developing new diagnostics and therapeutics is paramount to keeping TB under control. However, it largely depends upon understanding the pathogenic mechanisms of <em>Mycobacterium tuberculosis</em> (Mtb), the causative agent of TB. Mtb is an intracellular pathogen capable of subverting the defensive functions of the immune cells, and it can survive and multiply within humans' mononuclear phagocytes. Emerging evidence indicates that long non-coding RNAs (lncRNAs), a class of RNA molecules with limited coding potential, are critical players in this intricate game as they regulate gene expression at transcriptional and post-transcriptional levels and also by chromatin modification. Moreover, they have been shown to regulate cellular processes by controlling the function of other molecules, such as DNA, RNA, and protein, through binding with them. Recent studies have shown that lncRNAs are differentially regulated in the tissues of TB patients and cells infected in vitro with Mtb. Some dysregulated lncRNAs are associated with essential roles in modulating immune response, apoptosis, and autophagy in the host cells, adding a new dimension to TB pathogenesis. In this article, we provide a comprehensive review of the recent literature in this field and the impact of lncRNAs in unraveling pathogenic mechanisms in TB. We also discuss how the studies involving lncRNAs provide insight into TB pathogenesis, especially Mtb-host interactions.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 281-293"},"PeriodicalIF":5.9,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143129808","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":"LINC00323 knockdown suppresses the proliferation, migration, and vascular mimicry of non-small cell lung cancer cells by promoting ubiquitinated degradation of AKAP1","authors":"Bin Ke ,&nbsp;Hai Zhong ,&nbsp;Yuxin Gong ,&nbsp;Xiaofei Chen ,&nbsp;Chenxin Yan ,&nbsp;Lin Shi","doi":"10.1016/j.ncrna.2024.12.006","DOIUrl":"10.1016/j.ncrna.2024.12.006","url":null,"abstract":"<div><h3>Background</h3><div>LINC00323, a new long noncoding RNA, is aberrantly expressed in several cancers. However, the expression, function, and mechanism of LINC00323 in non-small cell lung cancer (NSCLC) are unclear.</div></div><div><h3>Methods</h3><div>In the present study, LINC00323, VEGFA, microvessel density (MVD), and AKAP1 levels were confirmed in NSCLC tissues. Cell proliferation, migration, and vascular mimicry (VM) were examined to assess the effects of LINC00323 and AKAP1 on NSCLC cells. In addition, the interaction between LINC00323 and AKAP1 was verified by RNA pull-down, LC-MS/MS and RNA immunoprecipitation. The ubiquitination level of AKAP1 was also confirmed through coimmunoprecipitation, cycloheximide (CHX) chase, and ubiquitination assays in vitro.</div></div><div><h3>Results</h3><div>Our results revealed that LINC00323 was upregulated in NSCLC tissues and was positively correlated with metastasis, poor prognosis, VEGFA expression, elevated MVD, and AKAP1 expression. Functionally, LINC00323 or AKAP1 knockdown suppressed the proliferation, migration, and VM of NSCLC cells. Mechanistically, LINC00323 could target AKAP1, and LINC00323 knockdown accelerated ubiquitination-mediated AKAP1 protein degradation. Moreover, LINC00323 silencing suppressed NSCLC cell progression by downregulating AKAP1.</div></div><div><h3>Conclusions</h3><div>LINC00323 knockdown prevents NSCLC cell proliferation, migration, and VM formation by targeting AKAP1, indicating that LINC00323 and AKAP1 might be biological targets for NSCLC treatment.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 131-140"},"PeriodicalIF":5.9,"publicationDate":"2024-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11720444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972500","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":"Targeting microRNA methylation: Innovative approaches to diagnosing and treating hepatocellular carcinoma","authors":"Albert Sufianov ,&nbsp;Murad Agaverdiev ,&nbsp;Andrey Mashkin ,&nbsp;Tatiana Ilyasova","doi":"10.1016/j.ncrna.2024.12.002","DOIUrl":"10.1016/j.ncrna.2024.12.002","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) stands as the most prevalent form of primary liver cancer and is frequently linked to underlying chronic liver conditions such as hepatitis B, hepatitis C, and cirrhosis. Despite the progress achieved in the field of oncology, HCC remains a significant clinical challenge, primarily due to its typically late-stage diagnosis and the complex and multifaceted nature of its tumor biology. These factors contribute to the limited effectiveness of current treatment modalities and result in poor patient prognosis. Emerging research has underscored the vital role of microRNAs (miRNAs)—small, non-coding RNA molecules that play a pivotal part in the post-transcriptional regulation of gene expression. These miRNAs are integral to a wide array of cellular functions, including proliferation, apoptosis, and differentiation, and their dysregulation is closely associated with the pathogenesis of various cancers, notably HCC. A major focus in recent studies has been on the epigenetic regulation of miRNAs through methylation, a key mechanism that modulates gene expression. This process, involving the addition of methyl groups to CpG islands in the promoter regions of miRNA genes, can result in either gene silencing or activation, influencing the expression of oncogenes and tumor suppressor genes. Such alterations have profound implications for tumor growth, metastasis, and resistance to treatment. Evidence suggests that aberrant miRNA methylation can serve as a powerful biomarker for early detection and prognosis in HCC and may present novel opportunities for therapeutic intervention. This review aims to provide a comprehensive overview of the current landscape of miRNA methylation in HCC, elucidating its significance in the molecular mechanisms of liver cancer and examining its potential for clinical application. By exploring the diagnostic and therapeutic potential of miRNA methylation, we seek to highlight its value in enhancing personalized treatment strategies and improving patient outcomes.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 150-157"},"PeriodicalIF":5.9,"publicationDate":"2024-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11742574/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143013428","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":"Decoding the regulatory roles of circular RNAs in cardiac fibrosis","authors":"Qianhui You ,&nbsp;Jiajing Yu ,&nbsp;Runfang Pan,&nbsp;Jiaming Feng,&nbsp;Haidong Guo,&nbsp;Baonian Liu","doi":"10.1016/j.ncrna.2024.11.007","DOIUrl":"10.1016/j.ncrna.2024.11.007","url":null,"abstract":"<div><div>Cardiovascular diseases (CVDs) are the primary cause of death globally. The evolution of nearly all types of CVDs is characterized by a common theme: the emergence of cardiac fibrosis. The precise mechanisms that trigger cardiac fibrosis are still not completely understood. In recent years, a type of non-coding regulatory RNA molecule known as circular RNAs (circRNAs) has been reported. These molecules are produced during back splicing and possess significant biological capabilities, such as regulating microRNA activity, serving as protein scaffolds and recruiters, competing with mRNA, forming circR-loop structures to modulate transcription, and translating polypeptides. Furthermore, circRNAs exhibit a substantial abundance, notable stability, and specificity of tissues, cells, and time, endowing them with the potential as biomarkers, therapeutic targets, and therapeutic agents. CircRNAs have garnered growing interest in the field of CVDs. Recent investigations into the involvement of circRNAs in cardiac fibrosis have yielded encouraging findings. This study aims to provide a concise overview of the existing knowledge about the regulatory roles of circRNAs in cardiac fibrosis.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 115-130"},"PeriodicalIF":5.9,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11697406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932942","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":"Non-coding RNAs and regulation of the PI3K signaling pathway in lung cancer: Recent insights and potential clinical applications","authors":"Mehrdad Hashemi ,&nbsp;Asal Abolghasemi Fard ,&nbsp;Bita Pakshad ,&nbsp;Pezhman Shafiei Asheghabadi ,&nbsp;Amineh Hosseinkhani ,&nbsp;Atena Sadat Hosseini ,&nbsp;Parham Moradi ,&nbsp;Mohammadreza Mohammadbeygi Niye ,&nbsp;Ghazal Najafi ,&nbsp;Mohadeseh Farahzadi ,&nbsp;Saloomeh Khoushab ,&nbsp;Afshin Taheriazam ,&nbsp;Najma Farahani ,&nbsp;Mahya Mohammadi ,&nbsp;Salman Daneshi ,&nbsp;Noushin Nabavi ,&nbsp;Maliheh Entezari","doi":"10.1016/j.ncrna.2024.11.006","DOIUrl":"10.1016/j.ncrna.2024.11.006","url":null,"abstract":"<div><div>Lung cancer (LC) is one of the most common causes of cancer-related death worldwide. It has been demonstrated that the prognosis of current drug treatments is affected by a variety of factors, including late stage, tumor recurrence, inaccessibility to appropriate treatments, and, most importantly, chemotherapy resistance. Non-coding RNAs (ncRNAs) contribute to tumor development, with some acting as tumor suppressors and others as oncogenes. The phosphoinositide 3-kinase (PI3Ks)/AKT serine/threonine kinase pathway is one of the most important common targets of ncRNAs in cancer, which is widely applied to modulate the cell cycle and a variety of biological processes, including cell growth, mobility survival, metabolic activity, and protein production. Discovering the biology of ncRNA-PI3K/AKT signaling may lead to advances in cancer diagnosis and treatment. As a result, we investigated the expression and role of PI3K/AKT-related ncRNAs in clinical characteristics of lung cancer, as well as their functions as potential biomarkers in lung cancer diagnosis, prognosis, and treatment.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 1-21"},"PeriodicalIF":5.9,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11665378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142886202","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-192–5p targets cell cycle regulation in diabetic kidney disease via cyclin-dependent kinase inhibitor 3","authors":"Biswajit Sahoo,&nbsp;Deendayal Das Mishra,&nbsp;Swasti Tiwari","doi":"10.1016/j.ncrna.2024.11.003","DOIUrl":"10.1016/j.ncrna.2024.11.003","url":null,"abstract":"<div><div>Diabetic kidney disease (DKD), a.k.a diabetic nephropathy, is a leading cause of end-stage renal disease. However, in a fair percentage of patients with type-2 diabetes, renal involvement also occurs due to non-diabetic reasons (non-diabetic kidney disease, NDKD). In this study, we identified miRNA-mRNA regulatory networks specific to human DKD pathogenesis. miRNA profiling of the renal biopsy from cases (DKD, n = 5), disease controls (T2DM with NDKD, n = 6), and non-diabetic, non-CKD controls (patients undergoing nephrectomy for renal cancer, n = 3) revealed 68 DKD-specific miRNA regulation. Sixteen target mRNAs of these DKD-miRNAs were found to have a negative association with the estimated glomerular filtration rate (eGFR) in patients with DKD. The renal gene expression and eGFR data of DKD patients (n = 10–18) in the NephroSeq database were used. Based on these findings, 11 miRNA-mRNA regulatory networks were constructed for human DKD pathogenesis. Of these, in-vitro validation of miR-192-5p- CDKN3 (Cell cycle-dependent kinase inhibitor 3) network was done as miR-192–5p exhibited a maximum number of target genes in the identified DKD regulatory networks, and CDKN3 appeared as a novel target of miR-192–5p in our study. We demonstrated that miR-192–5p overexpression or knockdown of CDKN3 attenuated high glucose-induced apoptosis, fibrotic gene expression, cell hypertrophy, and cell cycle dysregulation and improved viability of proximal tubular cells. Moreover, miR-192–5p overexpression significantly inhibited CDKN3 mRNA and protein expression in proximal tubular cells. Overall, 11 miRNA-mRNA regulatory networks were predicted for human DKD pathogenesis; among these, the association of miR-192-5p- CDKN3 network DKD pathogenesis was confirmed in proximal tubular cell culture.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 60-72"},"PeriodicalIF":5.9,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907842","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":"Deciphering the roles of non-coding RNAs in liposarcoma development: Challenges and opportunities for translational therapeutic advances","authors":"Zhi Xiong Chong ,&nbsp;Wan Yong Ho ,&nbsp;Swee Keong Yeap","doi":"10.1016/j.ncrna.2024.11.005","DOIUrl":"10.1016/j.ncrna.2024.11.005","url":null,"abstract":"<div><div>Liposarcoma is one of the most prevalent forms of soft tissue sarcoma, and its prognosis is highly dependent on its molecular subtypes. Non-coding RNAs (ncRNAs) like microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) can bind various cellular targets to regulate carcinogenesis. By affecting the expressions and activities of their downstream targets post-transcriptionally, dysregulations of miRNAs can alter different oncogenic signalling pathways, mediating liposarcoma progression. On the contrary, lncRNAs can sponge miRNAs to spare their downstream targets from translational repression, indirectly affecting miRNA-regulated oncogenic activities. In the past 15 years, multiple fundamental and clinical research has shown that different ncRNAs play essential roles in modulating liposarcoma development. Yet, there is a lack of an effective review report that could summarize the findings from various studies. To narrow this literature gap, this review article aimed to compare the findings from different studies on the tumour-regulatory roles of ncRNAs in liposarcoma and to understand how ncRNAs control liposarcoma progression mechanistically. Additionally, the reported findings were critically reviewed to evaluate the translational potentials of various ncRNAs in clinical applications, including employing these ncRNAs as diagnostic and prognostic biomarkers or as therapeutic targets in the management of liposarcoma. Overall, over 15 ncRNAs were reported to play essential roles in modulating different cellular pathways, including apoptosis, WNT/β-catenin, TGF-β/SMAD4, EMT, interleukin, and YAP-associated pathways to influence liposarcoma development. 28 ncRNAs were reported to be upregulated in liposarcoma tissues or circulation, whereas 11 were downregulated, making them potential candidates as liposarcoma diagnostic biomarkers. Among these ncRNAs, measuring the tissues or circulating levels of miR-155 and miR-195 was reported to help detect liposarcoma, differentiate liposarcoma subtypes, and predict the survival and treatment response of liposarcoma patients. Overall, except for a few ncRNAs like miR-155 and miR-195, current evidence to support the use of discussed ncRNAs as biomarkers and therapeutic targets in managing liposarcoma is mainly based on a single-center study with relatively small sample sizes or cell-based studies. Hence, more large-scale multi-center studies should be conducted to further confirm the sensitivity, specificity, and safety of ncRNAs as biomarkers and therapeutic targets. Instead of furthering investigation to confirm the translational values of all the discussed ncRNAs, which can be time- and cost-consuming, it would be more practical to focus on a few ncRNAs, including miR-155 and miR-195, to evaluate if they are sensitive and safe to be used as liposarcoma biomarkers and therapeutic agents or targets.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 73-90"},"PeriodicalIF":5.9,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907840","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 functions of immune system-derived miRNAs in cardiovascular diseases","authors":"Albert Sufianov ,&nbsp;Murad Agaverdiev ,&nbsp;Andrey Mashkin ,&nbsp;Tatiana Ilyasova","doi":"10.1016/j.ncrna.2024.11.004","DOIUrl":"10.1016/j.ncrna.2024.11.004","url":null,"abstract":"<div><div>Cardiovascular diseases (CVD) are the foremost cause of mortality worldwide, with recent advances in immunology underscoring the critical roles of immune cells in their onset and progression. MicroRNAs (miRNAs), particularly those derived from the immune system, have emerged as vital regulators of cellular functions within the cardiovascular landscape. This review focuses on \"immuno-miRs,\" a class of miRNAs that are highly expressed in immune cells, including T cells, B cells, NK cells, neutrophils, and monocytes/macrophages, and their significant role in controlling immune signaling pathways. Highlighting recent studies in human and animal models, this review examines how miRNAs influence both innate and adaptive immune responses and explores their potential as therapeutic targets for CVD. Special emphasis is placed on miRNAs that regulate T cells, suggesting that targeted manipulation of these miRNA pathways could offer new strategies for CVD treatment. As research in cardiovascular immunology advances, this review aims to provide a thorough overview of the potential of immune system-derived miRNAs to revolutionize CVD management and therapy, addressing a major global health challenge.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 91-103"},"PeriodicalIF":5.9,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907776","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}