Cell Journal最新文献

{"title":"Maturation and Assembly Stages of IMPDH-Cytoophidia Induced by IMPDH Inhibition.","authors":"Zahra Salehi Dolabi, Yazdanparast Razieh","doi":"10.22074/cellj.2025.2047867.1745","DOIUrl":"https://doi.org/10.22074/cellj.2025.2047867.1745","url":null,"abstract":"<p><p>Inosine-5'-monophosphate dehydrogenase (IMPDH) serves as a key regulatory enzyme, catalyzing a crucial step in the de novo synthesis of guanine nucleotides. This enzyme plays a pivotal role in various cellular functions, including proliferation, differentiation, homeostasis, and metabolism. IMPDH has the unique ability to form protein polymer fibers known as IMPDH cytoophidia. These natural biological structures are integral to purine metabolism and play a significant role in regulating changes within the cellular environment. Utilizing advanced techniques such as immunofluorescence microscopy and Western blot analysis, we have demonstrated that ribavirin (RBV) exhibits remarkable efficacy in inducing time-dependent cytoophidia formation when compared to other IMPDH inhibitors. Our observations reveal that small filaments progressively aggregate into larger secondary structures, reaching their peak formation at 12 hours. Subsequently, the structures begin to decrease by 24 hours, and ringlike formations dominate the cellular landscape at a remarkable 62% incidence. These findings suggest a complex and dynamic process of cytoophidia maturation in response to prolonged and time-dependent IMPDH inhibition. This process underscores the sequential emergence and development of secondary structures that surpass the conventional ring-rod configuration. Our study provides valuable insights into the mechanisms underlying cytoophidia formation and their potential implications for cellular regulation and metabolism.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"27 1","pages":"1-7"},"PeriodicalIF":1.7,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145276323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>UBD</i> Promotes The Proliferation and Epithelial-Mesenchymal Transition of Hepatocellular Carcinomas via Regulating <i>CTNNA3</i>.","authors":"Yajin Wang, Yuqing Du","doi":"10.22074/cellj.2025.2045823.1724","DOIUrl":"https://doi.org/10.22074/cellj.2025.2045823.1724","url":null,"abstract":"<p><strong>Objective: </strong>Hepatocellular carcinoma (HCC), a prevalent and aggressive malignancy, is one of the most common malignancies worldwide. Various studies show that ubiquitin D (<i>UBD</i>) is overexpresses in different cancer types and may serve as a potential prognostic factor. Although catenin alpha 3 (<i>CTNNA3</i>) is a tumour suppressor in HCC, the relationship between <i>UBD</i> and <i>CTNNA3</i> in HCC remains unclear. This study aims to explore the role of <i>UBD</i> in HCC and its relationship with <i>CTNNA3</i> in HCC cells.</p><p><strong>Materials and methods: </strong>In this experimental study, <i>UBD</i> expression in clinical samples was analysed by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry. Protein levels of epithelialmesenchymal transition (EMT) markers were evaluated by Western blot. Cellular behaviours that included proliferation, colony formation, migration, and invasion were assessed using the CCK-8, colony formation, EdU, and transwell assays. UBD-mediated ubiquitination of CTNNA3 was examined by <i>in vitro</i> ubiquitination assays.</p><p><strong>Results: </strong>There was a significant elevation in <i>UBD</i> expression in the HCC patients, which correlated with poor prognosis. Knockdown of <i>UBD</i> suppressed the proliferation, colony formation, and EMT of the HCC cells. <i>UBD</i> reduced CTNNA3 expression in HCC cells by promoting the ubiquitination and degradation of CTNNA3. Decreased <i>CTNNA3</i> expression in HCC patients was associated with poor overall survival. Silencing of <i>CTNNA3</i> repressed HCC proliferation, migration, invasion, and EMT. <i>CTNNA3</i> deficiency counteracted the inhibitory effects of <i>UBD</i> knockdown on the malignant behaviour of the HCC cells.</p><p><strong>Conclusion: </strong><i>UBD</i> plays an oncogenic role in HCC by encouraging proliferation and EMT through promoting CTNNA3 degradation. These findings suggest that targeting the <i>UBD</i>/<i>CTNNA3</i> axis could be a potential therapeutic strategy for HCC management.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"27 1","pages":"1-10"},"PeriodicalIF":1.7,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145276380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Innovative Stem Cell-Based Therapeutic Modalities to Address Major Depression and Treatment-Resistant Depression: A Review.","authors":"Batoul Mirbolouk, Kosar Babaeian Roshani, Ali Bahari Golamkaboudi, Zahra Barabadi, Zeinab Malmasi, Massoud Vosough, Elham Vojoudi","doi":"10.22074/cellj.2025.2046068.1727","DOIUrl":"https://doi.org/10.22074/cellj.2025.2046068.1727","url":null,"abstract":"<p><p>Depression is among the most widespread mental health conditions worldwide, with a significant number of patients showing inadequate responses to pharmacological treatments. Despite the development of numerous pharmacological therapies over the past six decades, a substantial proportion of patients with major depressive disorder (MDD) remain unresponsive to conventional therapies, prompting the exploration of innovative therapeutic strategies. This review critically examines the potential of stem cell-based therapies as a novel alternative to conventional antidepressant treatments, with a particular focus on individuals diagnosed with MDD. This study explores the molecular pathways that mediate neuroinflammatory responses in MDD, emphasizing the contributions of key pro-inflammatory cytokines to impaired neuroplasticity, mitochondrial dysfunction, and heightened oxidative stress. In addition, this study discusses the immunomodulatory properties of mesenchymal stromal cells (MSCs), highlighting their capacity to enhance antiinflammatory signaling, promote neurogenesis, and restore neurotransmitter homeostasis. Moreover, this review underscores the neuroprotective role of MSCs in mitigating oxidative stress-induced neuronal injury, with particular emphasis on their ability to secrete neurotrophic factors such as brain-derived neurotrophic factor (BDNF), which support neuronal integrity and survival.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"27 1","pages":"1-12"},"PeriodicalIF":1.7,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Acute Myeloid Leukemia-Derived Extracellular Vesicles on Expression of <i>CTNNB1, TGF-β,</i> and <i>VEGF</i> Genes in Bone Marrow Mesenchymal Stem Cells: Insights into Leukemia Pathogenesis.","authors":"Zahra Nazari, Radman Mazloomnejad, Mohammadhossein Mohammadi, Mahdieh Mehrpouri","doi":"10.22074/cellj.2025.2040586.1667","DOIUrl":"https://doi.org/10.22074/cellj.2025.2040586.1667","url":null,"abstract":"<p><strong>Objective: </strong>Acute myeloid leukemia (AML) is a heterogeneous malignancy driven by disruptions in the bone marrow microenvironment (BME). Extracellular vesicles (EVs) are crucial communicators and effectors in the BME, facilitating interactions between leukemic cells and stromal components to promote leukemogenesis. Elucidating these EVmediated processes is essential for developing novel therapeutic strategies. This study sought to clarify the effects of EVs derived from newly diagnosed non-M3 AML patients on bone marrow mesenchymal stromal cells (BMSCs), focusing on proliferation, survival, apoptosis, and expression of <i>CTNNB1, TGF-β,</i> and <i>VEGF</i> genes, which are pivotal in leukemia progression.</p><p><strong>Materials and methods: </strong>In this experimental study, AML-derived EVs were isolated from 30 newly diagnosed non-M3 AML patients and characterized by dynamic light scattering (DLS), transmission electron microscopy (TEM), Bradford assay, and flow cytometry. BMSCs were isolated from healthy BM aspirates and were co-cultured with EVs at concentrations of 10, 40, and 60 μg/ml for 24, 48, and 72 hours. Outcomes were assessed using quantitative reverse transcription polymerase chain reaction (RT-PCR), (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliuom bromide (MTT) assay, flow cytometry [for apoptosis, reactive oxygen species (ROS), and Ki67], and Western blot analyses.</p><p><strong>Results: </strong>AML-derived EVs at 40 μg/ml significantly suppressed apoptosis, enhanced cell survival, and upregulated <i>CTNNB1, TGF-β,</i> and <i>VEGF</i> gene expression in BMSCs via the Wnt/β-catenin signaling pathway, as confirmed by increased β-catenin protein levels. However, a 60 μg/ml dose increased apoptosis and reduced gene expression.</p><p><strong>Conclusion: </strong>These findings can suggest that AML-derived EVs modulate the BME by promoting BMSC survival and upregulating pro-leukemic genes at an optimal dose, offering a potential therapeutic target for AML treatment.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"27 1","pages":"1-12"},"PeriodicalIF":1.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of Mertk Mutation and Development of A Polymerase Chain Reaction Genotyping Method in Royal College of Surgeons Rats.","authors":"Mahdi Hesaraki, Magid Fallahi, Behrouz Asgari Abibeiglou, Pouya Tavakol-Rad, Leila Satarian, Mohsen Basiri","doi":"10.22074/cellj.2025.2049419.1761","DOIUrl":"https://doi.org/10.22074/cellj.2025.2049419.1761","url":null,"abstract":"<p><p>The retinal pigment epithelium (RPE) cells are a single layer of cells with specific functions in vision. The <i>Mertk</i> gene, encoding a receptor tyrosine kinase, is critical for the phagocytic function of retinal RPE cells. Mutations in <i>Mertk</i> disrupt RPE function and contribute to retinal degeneration. This study aims to characterize the Mertk mutation in Royal College of Surgeons (RCS) rats and develop a polymerase chain reaction (PCR)-based method for genotyping these mutations to improve colony management. DNA was extracted from mutant <i>Mertk</i>^-/- and wild-type rats, followed by PCR amplification using primers flanking the deletion region. Sequencing of the PCR products was performed to identify the precise nature of the mutation. A PCR-based genotyping method was then developed to distinguish between homozygous and heterozygous mutants. Sequencing revealed a 1850 bp deletion in the <i>Mertk</i> gene, resulting in a truncated protein that potentially impairs RPE phagocytosis. The newly developed PCR method successfully differentiated between homozygous and heterozygous mutant rats. This genotyping technique proved to be efficient and reliable, facilitating the management of rat colonies for research purposes. This study provides a detailed molecular characterization of the Mertk mutation in RCS rats, enhancing our understanding of <i>Mertk</i>-related retinal degenerative diseases. The development of a robust PCR-based genotyping method enables efficient differentiation of rat genotypes, aiding in the creation and maintenance of rat models for future research. These findings underscore the importance of molecular characterization in advancing our understanding of genetic models and improving research meth odologies.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"27 1","pages":"1-5"},"PeriodicalIF":1.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-129-5p Modulates <i>Fndc5</i> Expression in Adipose Tissue of Diabetic Mice.","authors":"Farzaneh Rabiee, Leyla Maleki, Navid Abedpoor, Mohammad Hossein Nasr-Esfahani","doi":"10.22074/cellj.2025.2050213.1772","DOIUrl":"https://doi.org/10.22074/cellj.2025.2050213.1772","url":null,"abstract":"<p><strong>Objective: </strong>The study aims to investigate the regulatory mechanism of the <i>Fndc5</i> gene in subcutaneous adipose tissue of diabetic mice, with a focus on the role of miR-129-5p in the pathogenesis of type 2 diabetes mellitus (T2DM). Specifically, it examines how the dysregulation of miR-129-5p affects <i>Fndc5</i> expression and contributes to diabetesrelated metabolic changes. By exploring these molecular pathways, the research seeks to enhance our understanding of T2DM and identify potential therapeutic targets for its complications.</p><p><strong>Materials and methods: </strong>In this experimental study, a total of 12 C57BL/6 male mice (6 weeks old) were divided into control and 60% high-fat enriched advanced glycation end products (60% HF-AGE) groups (n=6 per group). Bioinformatics analysis involved mining altered miRNAs in type 2 diabetes and predicting miRNA interactions with <i>Fndc5</i> mRNA. RNA and proteins extracted from adipose tissue analyzed by using quantitative real-time polymerase chain reaction (PCR) and immunoblotting, respectively. The dual luciferase reporter assay investigated direct interaction between miR-129-5p and the <i>Fndc5</i> gene using HEK293T cells transfected with relevant vectors.</p><p><strong>Results: </strong>In mice receiving a 60% HF-AGE diet, significant increases in energy intake, body weight, insulin levels, and fasting blood glucose (FBS) were observed. Furthermore, miR-129-5p was identified as a potential regulator of the Fndc5 gene, displaying elevated expression in diabetic adipose tissue. Plasmid construction confirmed the binding site of miR-129-5p on the <i>Fndc5</i> 3'UTR, while dual luciferase assays validated its direct targeting of the Fndc5 transcript. This interaction corresponded with a reduced expression of <i>Fndc5</i>, highlighting its potential role in diabetes-related metabolic dysregulation.</p><p><strong>Conclusion: </strong>The upregulation of mir-129-5p in these tissues and the subsequent decrease in the expression of the <i>Fndc5</i> gene may play a role in developing pathological conditions in this tissue. These findings highlight potential mechanisms linking diet-induced diabetes with <i>Fndc5</i> regulation through miR-129-5p.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"27 1","pages":"1-10"},"PeriodicalIF":1.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comments on: The Geographical Distribution of Global Biobanks.","authors":"Nazli Servatian, Masoumeh Nouri","doi":"10.22074/cellj.2025.2054279.1800","DOIUrl":"https://doi.org/10.22074/cellj.2025.2054279.1800","url":null,"abstract":"","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"27 1","pages":"1-2"},"PeriodicalIF":1.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application of Amniotic Membrane to Effectively Treat Chronic Cervicitis: A Case Series.","authors":"Hanieh Najafiarab, Farah Farzaneh, Amirreza Keyvanfar, Niki Talebian","doi":"10.22074/cellj.2025.2047384.1739","DOIUrl":"https://doi.org/10.22074/cellj.2025.2047384.1739","url":null,"abstract":"<p><p>Chronic cervicitis is a clinical syndrome characterized by persistent inflammation of the cervical epithelium. Women with chronic cervicitis often experience symptoms such as vaginal discharge, dyspareunia, post-coital bleeding, and fatigue. The treatment of chronic cervicitis is controversial, particularly in cases where no specific pathogenic agent be identified. Natural wound dressings with human amniotic membranes have been successfully used in tissue healing procedures. Thus, this approach may be a potential therapeutic option for patients suffering from chronic cervicitis. This case series reports on five women diagnosed with chronic cervicitis. These patients had negative Pap smears, human papillomavirus (HPV) typing tests, and colposcopic biopsies, indicating no infections or malignancies. Despite receiving oral antibiotics, their symptoms did not improve, leading to the decision to treat them with amniotic membrane. The cervix was assessed using a speculum, and amniotic membranes manufactured by Sinacell Company were inserted into the affected cervical areas. The patients were instructed to avoid sexual intercourse for one week and continue using oral antibiotics. At the follow-up, all patients significantly improved without any adverse events. Additionally, colposcopic examinations revealed that most patients showed improvement in cervical inflammation and bleeding. The amniotic membrane can assist women with chronic cervicitis by alleviating symptoms and enhancing the healing of cervical ulcers without complications.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"27 1","pages":"1-8"},"PeriodicalIF":1.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Possible Role of N-Methyl-D-Aspartate Glutamate Receptors in The Induction of Acrosome Reaction in Human Sperm.","authors":"Hamid Reza Momeni, Elham Farjad, Abolghasem Naiemi, Tahereh Etemadi, Mohammad Hussein Abnosi, Niloufar Darbandi","doi":"10.22074/cellj.2025.2043073.1690","DOIUrl":"https://doi.org/10.22074/cellj.2025.2043073.1690","url":null,"abstract":"<p><strong>Objective: </strong>Acrosome reaction is a receptor and Ca²⁺-dependent process. N-Methyl-D- aspartate (NMDA) glutamate receptors are expressed in the human sperm and are involved in the Ca²⁺ influx. Therefore, the present study aimed to investigate whether these receptors could be concerned with the induction of acrosome reaction in the human sperm.</p><p><strong>Materials and methods: </strong>In this experimental study, human spermatozoa were divided into five groups: i. Spermatozoa at 0 hour, ii. Control group, iii. Spermatozoa treated with NMDA glutamate receptor agonist (L-glutamate), iv. Spermatozoa treated with NMDA glutamate receptor antagonist and agonist (MK-801 and L-glutamate respectively), and v. Spermatozoa treated with non-NMDA glutamate receptor agonist (Kainic acid). Spermatozoa from groups of 2 to 5 were incubated in a Co₂ incubator for 60 minutes. To study the acrosome reaction in the different groups' the sperm samples were stained with <i>Pisum sativum</i>. In addition, cytosolic Ca²⁺ levels were assessed in the experimental groups. One-way ANOVA followed by Tukey's test was used to determine the statistical significance of the data. A P<0.05 was considered significant.</p><p><strong>Results: </strong>In the present study, applying L-glutamate significantly (P<0.001) induced an acrosome reaction compared to the control group. In the MK-801+ L-glutamate group, MK-801 could significantly (P=0.010) inhibit the induction of acrosome reaction compared to the L-glutamate group. The application of kainic acid did not affect the induction of acrosome reaction compared to the control group. In the L-glutamate group, cytosolic Ca²⁺ levels were significantly (P=0.044) increased when compared with the control group. The application of MK-801+ L-glutamate could significantly (P=0.047) reverse the effect of L-glutamate on cytosolic Ca²⁺ levels compared to the L-glutamate group.</p><p><strong>Conclusion: </strong>The results of the present study showed that NMDA glutamate receptors play an essential role not only in the increase of cytosolic Ca²⁺ levels but also in the induction of the acrosome reaction in human sperm.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"26 12","pages":"682-687"},"PeriodicalIF":1.7,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144545789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between <i>DNMT1</i> Gene Polymorphisms and Cancer Susceptibility: A Systematic Review and Meta-analysis.","authors":"Asma Khorshid Shamshiri, Maryam Alidoust, Fahimeh Afzaljavan","doi":"10.22074/cellj.2025.2045804.1716","DOIUrl":"https://doi.org/10.22074/cellj.2025.2045804.1716","url":null,"abstract":"<p><strong>Objective: </strong>For years, it has been acknowledged that cancer cells contribute to aberrant DNA methylation, an epigenetic alteration. DNA methyltransferase 1 (<i>DNMT1</i>) is a large multidomain protein critical DNMT in cells. Due to its significant function in epigenetic control, <i>DNMT1</i> is a viable candidate gene for cancer susceptibility. The relationships between <i>DNMT1</i> polymorphisms and cancer risk have been investigated; however, the outcomes are inconsistent. This metaanalysis aims to clarify the relationships between DNMT1 polymorphisms and cancer susceptibility.</p><p><strong>Materials and methods: </strong>PubMed, Web of Science, and Scopus databases were systematically searched using specific search terms to identify potentially eligible papers published before January 2025. Fixed-effects or randomeffects models were employed to calculate odds ratios (OR) and 95% confidence intervals (CI). The I² statistic and Egger's test were utilised to evaluate inter-study heterogeneity and assess the presence of publication bias among the included studies. All statistical analyses were conducted using MetaGenyo software.</p><p><strong>Results: </strong>A total of 776 articles were retrieved from PubMed, Scopus, and Web of Science databases. After full-text evaluation and applying the literature selection criteria, 23 articles were included as case-control studies that assessed the relationship between 23 polymorphisms in <i>DNMT1</i> and cancer risk were included. The <i>rs2228612, rs2228611, rs16999593</i>, and <i>rs10420321</i> single nucleotide polymorphisms (SNPs) were most frequently investigated. The <i>rs2228612</i> co-dominant model [P=0.037, OR=0.89, 95% CI (0.80-0.99)] and <i>rs2228611</i> dominant model [P<0.001, OR=1.32, 95% CI (1.14-0.53)] revealed a substantial association with cancer risk. Subgroup analysis showed an association between the <i>rs2228612</i> co-dominant [P=0.022, OR=0.58, 95% CI (0.74-0.98)] and recessive [P=0.046, OR=1.15, 95% CI (1.00-1.32)] models with gastrointestinal cancer and the <i>rs2228611</i> co-dominant model with breast cancer [P=0.024, OR=1.15, 95% CI (1.02-1.29)].</p><p><strong>Conclusion: </strong>Although the current study found a role for <i>DNMT1</i> polymorphisms in cancer risk, further high-quality studies are needed to validate these findings.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"26 12","pages":"669-681"},"PeriodicalIF":1.7,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144545788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}