International journal of molecular medicine最新文献

{"title":"Exosome‑mediated crosstalk between the cardiovascular and musculoskeletal systems: Mechanisms and therapeutic potential (Review).","authors":"Qingchen Li, Haoyang Gao, Xiaotong Ma, Ze Wang, Linlin Zhao, Weihua Xiao","doi":"10.3892/ijmm.2025.5570","DOIUrl":"10.3892/ijmm.2025.5570","url":null,"abstract":"<p><p>The cardiovascular and musculoskeletal systems are two core systems essential for maintaining human physiological functions and their dynamic interactions play a critical role in overall health. Exosomes, nanosized vesicles released by cells, contain bioactive substances including microRNA, long non‑coding RNA, lipids and proteins and participate in the pathophysiological regulation of multiple organ systems by mediating intercellular communication. Bone‑derived exosomes ameliorate cardiovascular diseases through the regulation of oxidative stress, inflammatory responses and apoptosis. Conversely, cardiovascular‑derived exosomes enhance bone homeostasis by suppressing osteoclast activity or promoting osteogenic differentiation, but they may also exacerbate pathological progression in conditions such as osteoarthritis. Skeletal muscle‑derived exosomes protect cardiomyocytes in muscular dystrophy through functional molecules delivery. However, under pathological conditions such as sarcopenia, skeletal muscle‑derived exosomes may aggravate cardiac dysfunction by activating pro‑apoptotic signals. Similarly, cardiovascular‑derived exosomes exhibit dual roles in skeletal muscle regulation, promoting regeneration while potentially inducing atrophy during heart failure. In addition, exosomes demonstrate significant clinical value as diagnostic biomarkers and targeted drug delivery vehicles, both for early disease detection and regenerative therapies. The present review systematically outlined the mechanisms underlying exosome‑mediated bidirectional crosstalk between the cardiovascular and musculoskeletal systems and explores their clinical application potential. It provided theoretical insights and novel perspectives for further research into the pathogenesis and therapeutic strategies of cardiovascular and musculoskeletal diseases.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GW8510 alleviates muscle atrophy and skeletal muscle dysfunction in mice through AMPK/PGC1α signaling.","authors":"Yutong Chen, Zurui Liu, Chen Liu, Daqian Yang, Mengmeng Xiao, Zhengqian Li, Zhengwei Xie","doi":"10.3892/ijmm.2025.5569","DOIUrl":"10.3892/ijmm.2025.5569","url":null,"abstract":"<p><p>Preventing and restoring muscle loss and function is essential for elderly individuals. GW8510 may accelerate myotube differentiation. The present study aimed to investigate the protective effect of GW8510 (a CDK2 inhibitor) on muscle atrophy. Mouse models of muscle atrophy were induced by denervation, dexamethasone and glycerol. Muscle‑to‑body weight ratio, the cross‑sectional area of muscles, grip strength, fatigue and serum levels of superoxide dismutase and creatine kinase were assessed. <i>In vitro</i>, a dexamethasone‑induced C2C12 myotube atrophy model was used to evaluate mitochondrial function. Reverse transcription‑quantitative PCR, immunoblotting and small interfering RNA transfection were performed to explore the potential molecular mechanisms following treatment with GW8510. GW8510 resulted in a significant increase in the gastrocnemius and soleus muscle ratios in denervation mice (7 and 3%, respectively), alongside an increase in cross‑sectional area. Moreover, GW8510 significantly improved grip strength and superoxide dismutase activity, with similar protective effects in dexamethasone‑ and glycerol‑induced muscle atrophy models. GW8510 decreased reactive oxygen species production, increased mitochondrial DNA copy number, maintained mitochondrial dynamics and enhanced antioxidant activity in C2C12 myotubes. Mechanistically, GW8510 significantly inhibited the expression of atrophy‑associated markers F‑box protein 32 and tripartite motif‑containing 63 while activating AMPK (both P<0.01). The knockdown peroxisome proliferator‑activated receptor‑γ co‑activator‑1α (Pgc1α) negated the effects of GW8510. Overall, GW8510 mitigated muscle atrophy via the activation of the AMPK/PGC1α pathway. GW8510 could serve as a novel therapeutic agent for the prevention of muscle atrophy.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances of exosome regulating‑FXR to repair inflammatory bowel disease (Review).","authors":"Peter Muro, Caihong Jing, Yaru Qiao, Wenbing Wang, Bo Wang, Fei Mao","doi":"10.3892/ijmm.2025.5576","DOIUrl":"10.3892/ijmm.2025.5576","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD), which encompasses ulcerative colitis and Crohn's disease, poses significant treatment difficulties because of its persistent course and underlying inflammatory mechanisms. Existing treatments primarily focus on alleviating symptoms, while novel biological drugs that target specific molecular pathways could address the root causes of the disease. One such pathway involves the farnesoid X receptor (FXR), a nuclear receptor essential for bile acid metabolism, intestinal homeostasis and modulation of inflammation. Activating FXR can reduce intestinal inflammation and improve gut barrier function, highlighting its potential as a treatment target for IBD. However, using synthetic agonists to directly activate FXR has drawbacks, including off‑target effects and limited effectiveness. Exosomes, tiny nanoscale vesicles involved in cell‑to‑cell communication, have emerged as promising therapeutic tools for regulating FXR signaling in IBD. Exosomes, particularly those derived from mesenchymal stem cells, can deliver bioactive molecules that promote FXR activation, reduce inflammation, and enhance tissue regeneration. The present review examines how exosomes regulate FXR signaling and their potential therapeutic use in IBD. It covers exosome biogenesis, therapeutic benefits and their molecular mechanisms in IBD.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiota metabolites affect sleep as drivers of brain‑gut communication (Review).","authors":"Hanxing Cheng, Wanying Yang, Huaiyi Xu, Wenwen Zhu, Ailin Gong, Xuemei Yang, Sen Li, Houping Xu","doi":"10.3892/ijmm.2025.5571","DOIUrl":"10.3892/ijmm.2025.5571","url":null,"abstract":"<p><p>Sleep plays a crucial role in maintaining and improving physical and mental health. However, the prevalence of sleep disorders is increasing in modern society. Recently, the gut‑brain axis has emerged as a prominent focus within the realm of sleep disorder research, with gut microbiota metabolites serving as essential factors in gut‑brain communication. The present study summarizes the emerging connections between gut microbiota metabolites and sleep, mainly focusing on those derived from tryptophan and dietary fiber metabolism. It discusses potential pathways and molecular processes by which sleep interacts with the gut microbiota metabolites, aiming to evaluate the feasibility of using gut microbiota interventions to treat sleep disorders.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Egr‑1 promotes the proliferation and migration of vascular smooth muscle cells by transcriptionally activating Egr‑2 in arteriovenous fistulas.","authors":"Ke Hu, Shichen Bu, Yi Guo, Yuxuan Li, Shiwen Yu, Lulu Wang, Chuanqi Cai, Yiqing Li, Xin Liu, Hegui Huang, Weici Wang","doi":"10.3892/ijmm.2025.5568","DOIUrl":"10.3892/ijmm.2025.5568","url":null,"abstract":"<p><p>Arteriovenous fistulas (AVFs) are preferred access points for hemodialysis. The present study aimed to investigate the function of early growth response‑1 (Egr‑1) in the proliferation and migration of smooth muscle cells (SMCs) and assess its potential as a new therapeutic target for AVF treatment. A comprehensive analysis combining public data‑source mining, human tissue collection, animal studies, cell culture experiments and various molecular biology techniques was conducted. The public dataset GSE119296 was used for immunohistochemical analyses of human AVF stenosis samples. SMC‑specific Egr‑1 knockout mice and various in vitro assays on primary rat vascular SMCs were used to evaluate the effect of Egr‑1 on the functional capacity of SMCs. RNA sequencing and chromatin immunoprecipitation sequencing was performed. Egr‑1 was upregulated in human AVF stenosis samples and cultured SMCs. Knockout of Egr‑1 in mice mitigated AVF outflow tract stenosis, improved flow dynamics and diminished neointima formation. <i>In vitro</i>, Egr‑1 ablation reduced SMC proliferation and migration; Egr‑1 transcriptionally activated Egr‑2. Increased Egr‑1 expression facilitated SMC proliferation and migration through Egr‑2 regulation, contributing to AVF stenosis. Consequently, targeting Egr‑1 may offer a novel therapeutic approach for managing AVF intimal hyperplasia and improving AVF patency and function in patients with end‑stage renal disease.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SENP1 promotes p27kip1 nuclear export though enhanced SUMOylation in cholangiocarcinoma leading to increased cell proliferation and chemoresistance.","authors":"Kainian Jiang, Wei Yang, Jie Huang, Xiaolong Tan, Yan Liu, Saiya Tu, Jian Luo","doi":"10.3892/ijmm.2025.5582","DOIUrl":"10.3892/ijmm.2025.5582","url":null,"abstract":"<p><p>SUMOylation is a critical post‑translational modification, serving as a key role in nucleocytoplasmic translocation, transcriptional cofactor stabilization and modulation of chromatin remodeling factors, which are associated with oncogenesis, tumor progression and chemotherapy resistance in various types of cancer. SUMOylation was performed by small ubiquitin‑like modifier (SUMO), a kind of small ubiquitin‑like modifier, which was attached or removed from the substrates. The excessive export of nuclear p27kip1 induced by SUMOylation is associated with cell proliferation and chemotherapy resistance in cholangiocarcinoma (CCA). However, the exact underlying mechanism remains currently unknown. The present study investigated SUMO specific peptidase 1 (SENP1), which is known to participate in SUMOylation by activating nuclear SUMO1 precursors and deSUMOylating cytoplasmic substrates. SENP1 exhibited increased expression levels in CCA specimens compared with that in adjacent non‑cancerous tissues, as confirmed by bioinformatics analysis and immunohistochemical assays. A significant correlation between SENP1 and p27kip1 expression levels was observed. SENP1 overexpression significantly increased cytoplasmic p27kip1 expression levels, thereby promoting CCA cell proliferation, accelerating the G1‑S cell cycle transition and reducing chemical sensitivity through increasing overall SUMOylation of p27kip1, as confirmed via western blotting, immunofluorescence, flow cytometry, Cell Counting Kit‑8, 5‑ethynyl‑2'‑deoxyuridine incorporation and SUMOylation tests. By contrast, SENP1 knockdown demonstrated the opposite results. Subsequently, the use of ML‑792, COH000 and leptomycin B treatments, and the mutant variant SENP1‑C603A demonstrated that SENP1 regulates the functionality of p27kip1 through nuclear SUMOylation rather than cytoplasmic deSUMOylation. The involvement of SENP1 represents a pivotal role in governing the nucleocytoplasmic shuttling of p27kip1. SENP1 knockdown could effectively impede CCA cell proliferation and enhance the chemosensitivity of cis‑platinum by modulating the nuclear export of p27kip1 through SUMOylation, thus offering a potential therapeutic approach for CCA in the future.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipid metabolism in microglia: Emerging mechanisms and therapeutic opportunities for neurodegenerative diseases (Review).","authors":"Yunlong Sun, Kaifang Wei, Xudong Liao, Jian'an Wang, Li'na Gao, Bo Pang","doi":"10.3892/ijmm.2025.5580","DOIUrl":"10.3892/ijmm.2025.5580","url":null,"abstract":"<p><p>Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis, are characterized by progressive neuronal loss and neuroinflammation, with microglial dysfunction emerging as a central driver of pathogenesis. Microglia, the central nervous system‑resident immune cells, exhibit dual pro‑inflammatory and anti‑inflammatory phenotypes, dynamically regulated by lipid metabolic reprogramming. Chronic activation of M1 microglia exacerbates neuronal damage, while M2 microglia promote tissue repair via phagocytic clearance and neurotrophic factor secretion. Lipid dysregulation‑marked by ceramide accumulation, cholesterol esterification defects and oxidized lipid‑driven neuroinflammation‑critically modulates microglial polarization. Mechanistic studies reveal that mitochondrial dysfunction, lysosomal stress and ferroptosis intersect with lipid metabolic pathways to amplify neurotoxicity. Therapeutic strategies targeting lipid homeostasis, such as TREM2 agonism, demonstrate efficacy in preclinical models by restoring microglial function and mitigating pathology. This review synthesizes emerging evidence linking microglial lipid metabolism to NDD progression, highlighting novel biomarkers and therapeutic avenues to disrupt the lipid‑neuroinflammation axis in neurodegeneration.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated multi‑omics analysis of liver metabolic dysregulation in ACE2 knockout mice.","authors":"Shuai Xiao, Jinxiu Guo, Bo Yu, Shiyuan Zhao, Yicun Shang, Ni Li, Jiyao Cui, Fangqiang Song, Pei Jiang","doi":"10.3892/ijmm.2025.5575","DOIUrl":"10.3892/ijmm.2025.5575","url":null,"abstract":"<p><p>The present study systematically investigated the impact of angiotensin‑converting enzyme 2‑knockout (ACE2KO) on hepatic metabolic homeostasis and its molecular mechanisms using integrated transcriptomic, proteomic and metabolomic profiling. ACE2KO exacerbated hepatic lipid accumulation, as evidenced by elevated total cholesterol and triglyceride levels, while disrupting the renin‑angiotensin system equilibrium via increased angiotensin II levels and reduced angiotensin‑(1‑7) levels. Histopathological analysis revealed hepatocyte edema, vacuolar degeneration and inflammatory infiltration in the ACE2KO mice. Multi‑omics integration revealed systemic metabolic dysregulation. Transcriptomics identified 1,004 differentially expressed genes, including lipid metabolism regulators (Scd1 and Fabp1) and circadian rhythm modulators (Arntl and Cry1), proteomics identified 191 differentially expressed proteins associated with interferon signaling activation (Oas1a and Rsad2) and lipid synthesis suppression (Scd1 and Fasn), and metabolomics highlighted 193 differentially expressed metabolites indicative of bile acid dysregulation, glutathione redox imbalance and amino acid metabolism anomalies. Cross‑omics analysis indicated that ACE2 is a key regulator of metabolic homeostasis. Its absence causes systematic metabolic disorders, including lipid metabolism disorder, amino acid metabolic imbalance and detoxification dysfunction. These findings comprehensively delineated the multifaceted role of ACE2 in hepatic metabolic homeostasis, and provided mechanistic insights into and therapeutic targets for ACE2‑associated liver diseases.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TNF‑α induces premature senescence in tendon stem cells via the NF‑κB and p53/p21/cyclin E/CDK2 signaling pathways.","authors":"Hua Guo, Haixia Cao, Qian Lu, Zhifeng Gu, Guijuan Feng","doi":"10.3892/ijmm.2025.5581","DOIUrl":"10.3892/ijmm.2025.5581","url":null,"abstract":"<p><p>Achilles tendinitis (AT) is a complex disorder that affects tendon tissue and often responds poorly to non‑steroidal anti‑inflammatory drugs. Tumor necrosis factor‑α (TNF‑α), a proinflammatory cytokine involved in cell death and immune regulation, serves a central role in AT progression. The present study investigated the effects of TNF‑α on tendon stem cells (TSCs) and evaluated potential therapeutic strategies for AT. TNF‑α‑induced changes in TSCs were determined by investigating markers of cellular senescence, reactive oxygen species (ROS) activity, DNA damage and the expression of key transcription factors, including NF‑κB (phosphorylated‑p65, p65), p53, p21, cyclin E and CDK2. To determine whether TNF‑α‑induced senescence could be reversed, TSCs were treated with etanercept, a TNF‑α‑specific inhibitor. TNF‑α stimulation induced significant senescence in TSCs, as evidenced by increased ROS production, DNA damage and altered expression of senescence‑associated transcription factors. TNF‑α activated the NF‑κB and p53/p21/cyclin E/CDK2 signaling pathways, promoting TSC senescence. Etanercept treatment effectively reversed these effects, decreasing TSC senescence, suppressing inflammatory cell infiltration, decreasing TNF‑α protein expression and mitigating collagen fiber degradation. TNF‑α promotes TSCs senescence through specific signaling pathways and etanercept can counteract these deleterious effects. These results provide insights into the pathogenesis of AT and highlight TNF‑α inhibition as a promising therapeutic approach. Targeting TNF‑α may offer a novel treatment strategy for individuals with AT.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270418/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of MEX3A in tumorigenesis: Mechanisms, tumor‑specific effects and therapeutic implications (Review).","authors":"Lulu Tang, Li Zhang, Shun Yao, Xin Li, Yongfeng Wang, Qian Liu, Jiajia Li, Guorong Wen, Jiaxing An, Hai Jin, Jiaxing Zhu, Biguang Tuo","doi":"10.3892/ijmm.2025.5579","DOIUrl":"10.3892/ijmm.2025.5579","url":null,"abstract":"<p><p>Muscle excess 3A (MEX3A), a dual‑function RNA‑binding protein with E3 ubiquitin ligase activity, is a pivotal regulator of tumorigenesis. By modulating mRNA stability, translation and targeted protein degradation, MEX3A orchestrates key oncogenic processes, including tumor stemness maintenance, proliferation, migration and immune evasion. MEX3A is aberrantly expressed in various malignancies, such as colorectal and breast cancer, hepatocellular carcinoma and glioblastoma, where it engages key signaling pathways, including the Wnt/β‑catenin, PI3K/AKT and NF‑κB pathways. Mechanistically, MEX3A directly regulates oncogenic and tumor suppressor transcripts, influencing the cell dynamics within the tumor microenvironment. Furthermore, MEX3A upregulation is associated with a poor prognosis and therapy resistance, highlighting its potential as a prognostic biomarker and therapeutic target. The present review aimed to summarize the molecular functions, tumor‑specific roles and translational relevance of MEX3A, bridging the gap between mechanistic insight and clinical applications. Future studies exploring MEX3A‑targeted interventions may reveal novel strategies for precision oncology.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}