Hereditas最新文献

{"title":"Mechanism of LINC00958 in ferroptosis of breast cancer through the SRSF1/GPX4 axis.","authors":"Shan Wang, Xinlu Liu, Xiaoli Hou, Wei Sun, Jiajie Chen, Yasen Cao, Hong Cheng","doi":"10.1186/s41065-025-00469-6","DOIUrl":"10.1186/s41065-025-00469-6","url":null,"abstract":"","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"110"},"PeriodicalIF":2.7,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12180173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333008","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":"Epithelial zinc finger protein in lung adenocarcinoma: prognostic biomarker with molecular and clinical implications.","authors":"Xiaofen Wen, Jianling Zhu, Didi Xi, Minna Chen, De Zeng, Wenwu Xue, Danxia Lin, Jiaxin Shen","doi":"10.1186/s41065-025-00476-7","DOIUrl":"10.1186/s41065-025-00476-7","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to evaluate the prognostic significance of epithelial zinc finger protein (EZF/KLF4) in lung adenocarcinoma (LAC) and explore its potential roles in tumor progression and immune regulation.</p><p><strong>Methods and materials: </strong>EZF expression and its associations with clinical characteristics were analyzed using TCGA and GEO datasets, and validated by immunohistochemistry in 25 paired LAC and adjacent normal tissues. Mechanistic insights were investigated through protein-protein interaction networks, gene set enrichment analysis (GSEA), DNA methylation profiling, and immune cell infiltration analysis via single-sample GSEA. A prognostic nomogram incorporating EZF expression, pT and pN stages, and residual tumor status was constructed using Cox regression modeling.</p><p><strong>Results: </strong>EZF expression was significantly downregulated in LAC tissues compared to normal tissues across multiple cohorts (P < 0.001), yet paradoxically associated with advanced tumor stages and worse overall, disease-specific, and progression-free survival. Functional analyses revealed EZF-associated pathways enriched in immune modulation. EZF expression correlated strongly with infiltrating immune cells, including NK cells, eosinophils, mast cells, and neutrophils. Hypomethylation of the EZF promoter was linked to poor prognosis. The constructed nomogram exhibited strong predictive accuracy for patient outcomes.</p><p><strong>Conclusion: </strong>EZF functions as a context-dependent regulator in LAC and may act as a prognostic biomarker by modulating tumor-immune interactions. These findings offer novel insights into the integration of molecular and immune features for personalized risk stratification and therapeutic guidance in LAC.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"106"},"PeriodicalIF":2.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12175355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325316","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":"circ-NOLC1 inhibits the development of cervical cancer by regulating miR-330-5p-PALM signaling axis.","authors":"Yali Duo, Cong Kang, Lei Zheng, Jing Wang, Zhongjie Liu, FengLing Bi, Lei Qiu, Ning Zhao","doi":"10.1186/s41065-025-00478-5","DOIUrl":"10.1186/s41065-025-00478-5","url":null,"abstract":"<p><strong>Background: </strong>Recent studies have increasingly demonstrated that circular RNAs (circRNAs) play significant roles in the occurrence and progression of cervical cancer (CC). In CC, circRNAs act as ceRNAs by sponging miRNAs to regulate genes associated with proliferation, migration, and apoptosis, exhibiting both promoting and inhibiting effects on tumor progression. The aim of this study was to clarify the role of hsa_circ_0019686 (named circ-NOLC1) in CC.</p><p><strong>Methods: </strong>By conducting an online GEO2R analysis of the expression profile GSE113696 in the GEO database, circ-NOLC1 was selected. The expression levels of circ-NOLC1 in CC cell lines were measured using real-time quantitative PCR (RT-qPCR). The role of circ-NOLC1 in CC was validated through both in vitro and in vivo gain-of-function assays. Bioinformatic analysis, combined with luciferase reporter and RNA Immunoprecipitation (RIP) assays, confirmed that circ-NOLC1 acts as a sponge for miR-330-5p and regulates the expression of paralemmin-1 (PALM). The role of the circ-NOLC1-miR-330-5p-PALM signaling axis in CC was elucidated through the rescue experiments. Relative gene expression levels were measured using RT-qPCR, while relative protein levels were assessed through immunohistochemistry (IHC). CCK-8, wound healing, Transwell, and flow cytometry assays were employed to evaluate CC cell proliferation, migration, and invasion, respectively.</p><p><strong>Results: </strong>The expression levels of circ-NOLC1 were dramatically downregulated in CC cells (P < 0.001). Up-regulation of circ-NOLC1 significantly inhibited cell proliferation (P < 0.001), migration (P < 0.01) and invasion (P < 0.01), while promoting cell apoptosis (P < 0.001). In vivo studies showed that up-regulation of circ-NOLC1 suppressed tumor growth (tumor volume: P < 0.001; tumor weight: P < 0.01). Additionally, miR-330-5p was found to be up-regulated in CC (P < 0.001), whereas PALM was downregulated in CC (P < 0.001). The up-regulation of circ-NOLC1 inhibited the expression of miR-330-5p (P < 0.001) and enhanced the expression of PALM (P < 0.001). Rescue experiments further demonstrated that the up-regulation of circ-NOLC1 inhibited CC cell proliferation (P < 0.001), migration (P < 0.001), invasion (P < 0.001), while promoting apoptosis (P < 0.001) through the regulation of the miR-330-5p-PALM pathway.</p><p><strong>Conclusion: </strong>The circ-NOLC1 inhibits CC development through regulating the miR-330-5p-PALM signaling axis. This finding reveals a novel mechanism and identifies potential therapeutic targets, emphasizing the necessity for further regulatory studies and clinical validation.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"108"},"PeriodicalIF":2.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12175339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325315","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":"Ilizarov-assisted periosteal distraction for refractory arteriovenous malformation ulcers: first clinical report in Asia.","authors":"Xiangyi Wu, Ren Cai, Mao Ye, Xitao Yang, Dachuan Sun, Yifeng Han, Xindong Fan, Jiaxue Zhu","doi":"10.1186/s41065-025-00479-4","DOIUrl":"10.1186/s41065-025-00479-4","url":null,"abstract":"<p><p>Refractory ulcers caused by high-flow arteriovenous malformations (AVMs) pose significant therapeutic challenges due to persistent tissue ischemia and shear stress-induced graft failure. Traditional embolization or flap reconstruction strategies often yield suboptimal outcomes, particularly in weight-bearing regions. We present a 28-year-old female with a non-healing dorsal foot AVM ulcer despite multiple embolizations and radical toe amputations. Genetic testing revealed a KRAS mutation, confirming a somatic etiology of AVM. After a debridement and local flap repair, we employed Ilizarov-assisted periosteal distraction to improve local perfusion. 75% of the wound epithelialized and the infection resolved within 4 weeks postoperatively, with granulation tissue covering the remainder. This case highlights the mechanobiological advantages of Ilizarov-based neovascular stimulation in AVM-related ischemic ulcers.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"107"},"PeriodicalIF":2.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12175424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325317","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":"Abnormal expression of miR-330-3p predicts post-prostatectomy urinary incontinence and regulates the function of urethral fibroblasts by targeting MMP2.","authors":"Xiaoying Feng, Yuanyuan Mi, Mengye Weng","doi":"10.1186/s41065-025-00475-8","DOIUrl":"10.1186/s41065-025-00475-8","url":null,"abstract":"<p><strong>Background: </strong>Post-prostatectomy urinary incontinence (PPUI) is a common complication for patients with prostate cancer after surgery. MicroRNA-330-3p (miR-330-3p) is down-regulated in stress urinary incontinence patients. However, its clinical role and regulatory mechanism in PPUI remain unknown.</p><p><strong>Objective: </strong>To assess the clinical significance of miR-330-3p in PPUI and to explore the potential mechanisms via matrix metalloproteinase 2 (MMP2) regulation.</p><p><strong>Methods: </strong>This study enrolled 135 ageing prostate cancer patients (86 without PPUI, 49 with PPUI). Reverse transcription PCR (RT-qPCR) was utilized to measure the levels of miR-330-3p, while Receiver operating characteristic (ROC) analysis was conducted to evaluate the predictive significance of miR-330-3p for PPUI. The proliferative of human urethral fibroblasts (HUFs) was assessed by Cell Counting Kit-8 (CCK-8) assay, while inflammatory cytokines were quantified via enzyme-linked immunosorbent assay (ELISA) kits. Western blot assay was employed to examine the protein levels of extracellular matrix (ECM) remodeling-related markers. The miR-330-3p/MMP2 interaction was validated by dual-luciferase assay.</p><p><strong>Result: </strong>miR-330-3p was significantly downregulated in PPUI patients, with low expression predicting PPUI. In HUFs, miR-330-3p overexpression inhibited IL-1β-induced hyperproliferation, inflammation, and ECM degradation. Overexpression of MMP2 counteracted the influence of miR-330-3p mimic on HUFs.</p><p><strong>Conclusion: </strong>miR-330-3p is a potential biomarker for PPUI and regulates the function of urethral fibroblasts by targeting MMP2.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"109"},"PeriodicalIF":2.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12175350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325314","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":"Prognostic analysis of bladder cancer with neddylation-related genes.","authors":"Huang Xiaolong, Deng Min, Zhang Sizhou, Hu Daorong, Pan Juncheng, Wang Yanjian, Li Jie Gu Hong, Zheng Ji, Wu Qingjian","doi":"10.1186/s41065-025-00463-y","DOIUrl":"10.1186/s41065-025-00463-y","url":null,"abstract":"<p><strong>Background: </strong>Previous studies have demonstrated a close association between neddylation modifications and tumor progression as well as alterations in the microenvironment. This study aimed to explore the role of neddylation in bladder cancer (BLCA) progression and its prognostic significance.</p><p><strong>Methods: </strong>Gene expression data from the TCGA database were analyzed to identify neddylation gene modules using the limma software package and weighted gene co-expression network analysis (WGCNA). Prognostic models based on neddylation-related genes were subsequently developed through LASSO and Cox regression analyses. Additionally, a protein-protein interaction (PPI) network, gene set enrichment analysis (GSEA), and BLCA single-cell sequencing data were utilized to explore the functional roles of hub genes in BLCA and their impact on biological pathways. The expression of these hub genes was further validated in clinical samples via RT-qPCR.</p><p><strong>Results: </strong>WGCNA analysis revealed 1412 neddylation-related hub genes. LASSO and Cox regression analyses subsequently identified six key genes: CUL1, PUM2, UBE2D3, HIF3A, COPS2, and DDB1. Transcriptomic data and RT-qPCR findings indicated that PUM2 and HIF3A exhibited high expression levels in normal tissues, while DDB1 showed increased expression in tumor tissues; no significant changes were observed for CUL1, COPS2, and UBE2D3. By integrating these gene expressions with significant clinical features, a prognostic model was constructed that demonstrated excellent diagnostic efficiency (AUC: 0.793 at 1 year, 0.792 at 3 years, and 0.773 at 5 years). In addition, single cell sequencing highlighted the potential role of these genes in modulating immune responses and mediating interactions between tumor cells and immune cells. GSEA also suggested that DDB1 may play a crucial role in orchestrating key biological processes associated with BLCA, particularly in activating apoptotic signaling pathways.</p><p><strong>Conclusion: </strong>The six neddylation-related genes (CUL1, PUM2, UBE2D3, HIF3A, COPS2, and DDB1) emerge as potential independent indicators of survival in patients with BLCA, and the constructed survival models exhibit significant diagnostic efficacy.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"105"},"PeriodicalIF":2.7,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12172356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309861","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-106b-5p improving the progression of chronic kidney disease by inhibiting the TGF-β/Smad pathway.","authors":"Qihao Ma, Li Xu, Peng Zhou, Bo Yang, Yong Li, Danan Sun","doi":"10.1186/s41065-025-00468-7","DOIUrl":"https://doi.org/10.1186/s41065-025-00468-7","url":null,"abstract":"<p><strong>Background: </strong>Chronic Kidney Disease (CKD) is a progressive disorder marked by renal impairment and declining kidney function.</p><p><strong>Aims: </strong>To investigate the expression of miR-106b-5p in CKD and its regulatory relationship with the TGF-β/Smad pathway.</p><p><strong>Methods: </strong>A total of 150 cases of CKD patients were selected as the observation group, while 100 healthy individuals served as the control group. Lipopolysaccharide (LPS) was utilized to induce damage to HK-2 cells. Real-time fluorescence PCR was used to detect the expression of genes. The CCK - 8 assay was utilized to evaluate cell proliferation, while flow cytometry was applied to measure the cell apoptosis rate.</p><p><strong>Results: </strong>miR-106b-5p is notably downregulated in CKD and exhibits a significant positive correlation with the eGFR in affected patients. Additionally, miR-106b-5p demonstrates a strong association with the levels of inflammatory factors in individuals with CKD. Furthermore, the expression of miR-106b-5p is reduced in LPS-induced HK-2 cells. Upregulation of miR-106b-5p can improve the inhibitory effect of LPS on the viability of HK-2 cells, reduce the apoptosis rate of cells, and alleviate the inflammatory response. miR-106b-5p serves as a negative regulatory factor within the TGF-β/Smad signaling pathway by directly targeting the pivotal receptor TGFBR2 and the downstream effectors SMAD2/3 within the TGF-β signaling cascade.</p><p><strong>Conclusions: </strong>miR-106b-5p ameliorates CKD progression by suppressing the TGF - β/Smad signaling pathway and could potentially be a therapeutic target for CKD.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"103"},"PeriodicalIF":2.7,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12164090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293639","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":"Astragaloside IV regulates FOXM1 deubiquitination to ameliorate trophoblast damage caused by high glucose.","authors":"Fan Li, Xiaofang Zhao","doi":"10.1186/s41065-025-00465-w","DOIUrl":"10.1186/s41065-025-00465-w","url":null,"abstract":"<p><strong>Background: </strong>Gestational diabetes mellitus (GDM) is a common metabolic complication during pregnancy that poses significant risks to both the pregnant woman and her fetus. Astragaloside IV (Ast IV) belongs to the class of triterpenoid saponins and exhibits important physiological roles in various aspects, including antidiabetic, antioxidant, and antiviral effects. The main objective of this study is to investigate the effects of Ast IV on trophoblast damage caused by high glucose (HG) and its underlying mechanism of action.</p><p><strong>Methods: </strong>Cell viability was determined by the CCK8 assay. The levels of oxidative stress in cells were determined by lactate dehydrogenase (LDH), malondialdehyde (MDA), and reactive oxygen species (ROS) kits. Ferroptosis in cells was assessed by the iron content kit. Gene expression levels were detected by real-time quantitative reverse transcription PCR (qRT-PCR) and western blot. The protein stability of Forkhead box protein M1 (FOXM1) was determined by the cycloheximide (CHX) assay. The ubiquitination level of FOXM1 was detected by the immunoprecipitation assay.</p><p><strong>Results: </strong>Ast IV alleviated the inhibitory effect of HG on the proliferation of HTR-8/SVneo cells and reduced HG-induced oxidative stress and ferroptosis. Ast IV was able to decrease the ubiquitination of FOXM1, thereby ensuring the stability of its expression. The overexpression of FOXM1 significantly mitigated the inhibitory effect of HG on the viability of HTR-8/SVneo cells and concurrently decreased the occurrence of HG-induced oxidative stress and ferroptosis processes. Conversely, knockdown of FOXM1 diminished the protective effect of Ast IV on HTR-8/SVneo cells.</p><p><strong>Conclusions: </strong>Ast IV ameliorates HG-induced trophoblast injury by modulating deubiquitination of FOXM1, which provides a new insight into the treatment of GDM.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"104"},"PeriodicalIF":2.7,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12166594/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293638","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":"Dauriporphine inhibited lung cancer cell viability, motility, and energy metabolism through the miR-424-5p/MAPK14 axis.","authors":"Yan-Jia Du, Jin-Peng Lv, Yao Fu, Meng Lan, Jing-Feng Li, Hui Zhang, Nan Wu","doi":"10.1186/s41065-025-00473-w","DOIUrl":"10.1186/s41065-025-00473-w","url":null,"abstract":"<p><strong>Background: </strong>Dauriporphine is a major ingredient of Manispernum daericum DC., which has been demonstrated to show wide anti-tumor activities. miR-424-5p, as a regulator of lung cancer, was hypothesized to serve as the therapeutic target for dauriporphine This study evaluated the potential of dauriporphine in treating lung adenocarcinoma and revealed the underlying molecular mechanism.</p><p><strong>Results: </strong>The anti-tumor effect of dauriporphine on lung adenocarcinoma was assessed in A549 cells, and it was found that dauriporphine significantly inhibited the viability of A549 cells in a concentration-dependent manner with the half maximal inhibitory concentration (IC₅₀) value of 10.57 µM. Dauriporphine induced decreasing cell growth, motility, and energy metabolism, indicating the anti-tumor effect of dauriporphine on A549 cells. Dauriporphine inducing elevated miR-424-5p levels, while silencing miR-424-5p significantly recovered cell viability, migration, and energy metabolism of A549 cells. Mitogen-activated protein Kinase 14 (MAPK14) was negatively regulated by miR-424-5p, and the knockdown of MAPK14 could reverse the protective effect of miR-424-5p on dauriporphine-treated A549 cells.</p><p><strong>Conclusion: </strong>Dauriporphine inhibited cell growth, metastasis, and glycolysis-related energy metabolism of lung adenocarcinoma cells via modulating miR-424-5p/MAPK14 axis. Dauriporphine can be considered in drug development for lung adenocarcinoma.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"101"},"PeriodicalIF":2.7,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12153179/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274652","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":"Overexpression of miR-671-3p alleviates postmenopausal osteoporosis by targeting GREM2 to activate BMP2/SMAD signaling pathway.","authors":"Yanlin Liang, Changqing Gu, Peng Wang, Changwen Gu, Hongwei Ma, Shujun Ren","doi":"10.1186/s41065-025-00467-8","DOIUrl":"10.1186/s41065-025-00467-8","url":null,"abstract":"<p><strong>Background: </strong>Increased fracture risk is linked to postmenopausal osteoporosis (PMOP), and elucidating the function of microRNAs (miRNAs) in this condition is vital for identifying individuals at high risk of fractures. This research focused on exploring the function and mechanism of miR-671-3p in PMOP.</p><p><strong>Methods: </strong>Using qRT-PCR, we measured the expression levels of miR-671-3p in the serum of PMOP patients and evaluated its predictive capacity for osteoporosis occurrence through Receiver Operating Characteristic (ROC) analysis. An in vitro model of MC3T3-E1 osteoblasts cultured under simulated microgravity (MG) was established to mimic the osteoporosis-related bone loss microenvironment. It was used to investigate miR-671-3p's regulatory effects on cell proliferation (CCK-8 assay), apoptosis (Annexin V/PI staining), and osteogenic differentiation (ALP activity and osteogenic marker mRNA levels). Dual luciferase reporter gene assays and RNA immunoprecipitation (RIP) experiments were performed to validate the interaction between miR-671-3p and GREM2.</p><p><strong>Results: </strong>miR-671-3p expression was reduced in PMOP patients and in MG-exposed MC3T3-E1 cells. miR-671-3p exhibited strong predictive power for early detection of PMOP. When miR-671-3p was overexpressed, it enhanced osteogenic differentiation and suppressed apoptosis in MC3T3-E1 cells. GREM2 was pinpointed as a target of miR-671-3p, which inhibited osteogenic differentiation in MC3T3-E1 cells and accelerated MG-induced apoptosis. By inhibiting GREM2 expression, overexpression of miR-671-3p activated the BMP2/SMAD signaling pathway.</p><p><strong>Conclusion: </strong>Reduced miR-671-3p expression may signal the presence of PMOP. By targeting GREM2 to activate the BMP2/SMAD pathway, miR-671-3p may stimulate osteogenic differentiation, foster bone formation, and prevent the onset of osteoporosis.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"102"},"PeriodicalIF":2.7,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12153117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274653","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}