Non-coding RNA Research最新文献

{"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":"2025-02-25","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":"2025-02-22","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":"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":"2025-02-21","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":"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":"2025-02-11","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":"Expression of miR-15b-5p and toll-like receptor4 as potential novel diagnostic biomarkers for hepatitis C virus-induced hepatocellular carcinoma","authors":"Amal Ahmed Mohamed ,&nbsp;Noha Nagah Amer ,&nbsp;Noha Osama ,&nbsp;Wael Hafez ,&nbsp;Ali Elsaid Abdelrahman Ali ,&nbsp;Mahmoud Maamoun Shaheen ,&nbsp;Ayman Abd Alhady Alkhalegy ,&nbsp;Eman Alsayed Abouahmed ,&nbsp;Shamel Mohamed Soaida ,&nbsp;Lamees A. Samy ,&nbsp;Ahmed El-Kassas ,&nbsp;Ivan Cherrez-Ojeda ,&nbsp;Rehab R El-Awady","doi":"10.1016/j.ncrna.2024.12.003","DOIUrl":"10.1016/j.ncrna.2024.12.003","url":null,"abstract":"<div><h3>Objectives</h3><div>Globally, hepatocellular Carcinoma (HCC) ranks seventh in women's cancer and fifth in men's cancer. Early identification can minimize mortality and morbidity. MicroRNAs and Toll-like receptors have been suggested as potential new biomarkers for HCC; Therefore, we explored Toll-like receptor 4 (TLR-4) and miRNA 15b-5p as new non-invasive HCC biomarkers and early detection approaches.</div></div><div><h3>Methodology</h3><div>In this case-control study, four primary groups were formed from 400 patients who participated in this study: 100 hepatitis C (HCV) patients without cirrhosis or HCC, 100 HCV with cirrhosis patients, 100 HCC and HCV patients, and 100 healthy controls. The HCC diagnosis was confirmed according to the American Association for the Study of Liver Disease (AASLD) Practice Guidelines. Triphasic computed tomography was used to assess the HCC tumor size. Real-time PCR was used to analyze miRNA 15b-5p and Toll-like receptor 4 (TLR-4) expression profiles.</div></div><div><h3>Results</h3><div>Significant diagnostic performance was achieved by miRNA 15b-5p in differentiating the HCC group from the control group, with 90 % sensitivity and 88 % specificity (AUC] 0.935, p &lt; 0.001), while TLR-4 had moderate diagnostic performance with 85 % sensitivity and 86 % specificity (AUC:0.885, p &lt; 0.001).</div></div><div><h3>Conclusions</h3><div>The ability of miR-15b-5p to recognize HCC was positive and it outperformed Toll-like receptor4. MiR-15b-5p has the potential to be a more precise and predictive biological marker for HCC than Toll-like receptor4. Future studies exploring different miRNAs and HCC cases from various etiologies are required to better understand the role of miRNAs in this disease and allow for more effective strategies.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"10 ","pages":"Pages 262-268"},"PeriodicalIF":5.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025175","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 “MiRNA expression affects survival in patients with obstructive sleep apnea and metastatic colorectal cancer” [Non-coding RNA research 10 (2025) 91–97]","authors":"Piera Soccio ,&nbsp;Giorgia Moriondo ,&nbsp;Giulia Scioscia ,&nbsp;Pasquale Tondo ,&nbsp;Giuseppina Bruno ,&nbsp;Guido Giordano ,&nbsp;Roberto Sabato ,&nbsp;Maria Pia Foschino Barbaro ,&nbsp;Matteo Landriscina ,&nbsp;Donato Lacedonia","doi":"10.1016/j.ncrna.2024.09.010","DOIUrl":"10.1016/j.ncrna.2024.09.010","url":null,"abstract":"","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"10 ","pages":"Page 261"},"PeriodicalIF":5.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907839","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-210 overexpression increases pressure overload-induced cardiac fibrosis","authors":"G. Zaccagnini ,&nbsp;D. Baci ,&nbsp;S. Tastsoglou ,&nbsp;I. Cozza ,&nbsp;A. Madè ,&nbsp;C. Voellenkle ,&nbsp;M. Nicoletti ,&nbsp;C. Ruatti ,&nbsp;M. Longo ,&nbsp;L. Perani ,&nbsp;C. Gaetano ,&nbsp;A. Esposito ,&nbsp;F. Martelli","doi":"10.1016/j.ncrna.2025.01.009","DOIUrl":"10.1016/j.ncrna.2025.01.009","url":null,"abstract":"<div><div>Aortic stenosis, a common valvular heart disease, can lead to left ventricular pressure overload, triggering pro-fibrotic responses in the heart. miR-210 is a microRNA that responds to hypoxia and ischemia and plays a role in immune regulation and in cardiac remodeling upon myocardial infarction. This study investigated the effects of miR-210 on cardiac fibrosis caused by pressure overload.</div><div>Using a mouse model with inducible miR-210 over-expression, we subjected mice to transverse aortic constriction (TAC) to induce pressure overload. Mice with miR-210 over-expression developed eccentric hypertrophy, heightened expression of hypertrophic markers (Nppa and Nppb) and increased cross sectional area of cardiomyocytes, impacting the free wall of the left ventricle. These findings suggest that miR-210 worsens cardiac dysfunction. Furthermore, miR-210 over-expression led to a more robust and sustained inflammatory response in the heart, increased interstitial and perivascular fibrosis, and activation of myofibroblasts. miR-210 also promoted angiogenesis. <em>In vitro</em>, cardiac fibroblasts over-expressing miR-210 showed increased adhesion, wound healing and migration capacity.</div><div>Our results demonstrate that miR-210 contributes to adverse cardiac remodeling in response to pressure overload, including eccentric hypertrophy, inflammation, and fibrosis.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"12 ","pages":"Pages 20-33"},"PeriodicalIF":5.9,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143403305","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":"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":"2025-01-27","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":"LURAP1L-AS1 long noncoding RNA promotes breast cancer progression and associates with poor prognosis","authors":"Radhakrishnan Vishnubalaji ,&nbsp;Dania Awata ,&nbsp;Nehad M. Alajez","doi":"10.1016/j.ncrna.2025.01.006","DOIUrl":"10.1016/j.ncrna.2025.01.006","url":null,"abstract":"<div><div>Long noncoding RNAs (lncRNAs) are emerging as critical regulators of cancer biology, yet their roles in breast cancer, particularly in triple-negative breast cancer (TNBC), remain incompletely understood. Through a custom siRNA library screen targeting TNBC-associated lncRNAs in MDA-MB-231 and BT-549 TNBC cell models, we identified LURAP1L-AS1 as a key modulator of TNBC progression. Survival analysis of TNBC patients demonstrated a significant association between elevated LURAP1L-AS1 expression and poor clinical outcomes.</div><div>LURAP1L-AS1 knockdown significantly impaired colony formation and organoid growth of TNBC models, associated with increased apoptosis thus highlighting its role in promoting tumorigenicity. RNA sequencing of LURAP1L-AS1-depleted cells revealed dysregulation of pathways related to cell proliferation, apoptosis, migration, and RNA processing. Bioinformatics analysis predicted LURAP1L-AS1 to function as a competitive endogenous RNA (ceRNA), sponging key microRNAs, such as miR-7a-5p, miR-101-3p, miR-181a-5p, and miR-27a-3p, thereby modulating oncogenes including EZH2, MCL1, and KRAS, which are linked to increased cancer cell survival, proliferation, and metastasis.</div><div>In addition to its role in TNBC, correlation analysis using breast cancer patient datasets revealed a significant association between LURAP1L-AS1 and ESR1 expression, suggesting its broader impact across breast cancer subtypes. Concordantly, LURAP1L-AS1 depletion inhibited estrogen receptor-positive (ER+) MCF7 breast cancer cells colony formation and organotypic growth.</div><div>Our findings establish LURAP1L-AS1 as a functional lncRNA that promotes breast cancer progression, highlighting its potential for use in RNA-based therapies for breast cancer.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"12 ","pages":"Pages 1-9"},"PeriodicalIF":5.9,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143092240","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":"Research progress on the interaction between intestinal flora and microRNA in pelvic inflammatory diseases","authors":"Shuhan Dong ,&nbsp;Yunpeng Du ,&nbsp;Haiyang Wang ,&nbsp;Wenhan Yuan ,&nbsp;Wenxia Ai ,&nbsp;Li Liu","doi":"10.1016/j.ncrna.2025.01.007","DOIUrl":"10.1016/j.ncrna.2025.01.007","url":null,"abstract":"<div><div>Pelvic inflammatory disease (PID) is a common infectious disease of the female upper reproductive tract, and its pathological basis is immune inflammatory response. The imbalance of gut microflora (GM) may lead to the development of inflammatory process. A large number of studies have shown that fecal microbiota transplantation, probiotics, bacteria, prebiotics, and dietary intervention may play a potential role in remodeling GM and treating diseases. MicroRNAs (miRNAs) are involved in cell development, proliferation, apoptosis and other physiological processes. In addition, they play an important role in the inflammatory process, participating in the regulation of proinflammatory and anti-inflammatory pathways. Differences in miRNA profiles may be PID diagnostic tools and serve as prognostic markers of the disease. The relationship between miRNA and GM has not been fully elucidated. Recent studies have shown the role of miRNA in the regulation and induction of GM dysbiosis. In turn, microbiota can regulate the expression of miRNA and improve the immune status of the body. Therefore, this review aims to describe the interaction between GM and miRNA in PID, and to find potential precise targeted therapy for PID.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 303-312"},"PeriodicalIF":5.9,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143129810","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}