Epigenetics最新文献

{"title":"PRMT1 promotes immune escape in hepatocellular carcinoma by regulating arginine methylation modification of MYC protein.","authors":"Han Zhou, Yang Wang, Dan Wang, Mei Zhang, Kaidi Wang, Chunhui Liu","doi":"10.1080/15592294.2025.2509044","DOIUrl":"10.1080/15592294.2025.2509044","url":null,"abstract":"<p><p>Arginine methyltransferase 1 (PRMT1) is widely recognized as an oncogene in various cancers. However, its specific role and underlying mechanisms in hepatocellular carcinoma (HCC) remain insufficiently understood. This study investigated the function of PRMT1 in HCC development and immune evasion. A comprehensive approach combining database analysis (including TCGA, The Human Protein Atlas, Kaplan-Meier Plotter, and TIMER2.0), molecular techniques (such as RT-qPCR, Western blot analysis, and co-immunoprecipitation), cell-based assays (including MTT, colony formation, transwell, and T cell killing assays), and <i>in vivo</i> models was employed to explore PRMT1's role in HCC. The findings revealed a marked upregulation of PRMT1 in both HCC clinical samples and cell lines. Depletion of PRMT1 inhibited cell proliferation and immune evasion while reducing cell migration and invasion. Mechanistically, PRMT1 was shown to interact with MYC, facilitating its arginine methylation and enhancing its protein stability. Moreover, re-expression of MYC significantly reversed the anti-tumour effects associated with PRMT1 depletion. <i>In vivo</i> experiments further corroborated these results. Collectively, PRMT1 promotes HCC progression and immune escape by mediating ADMA methylation of MYC, thereby regulating its stability and expression.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2509044"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The myoblast methylome: multiple types of associations with chromatin and transcription.","authors":"Sagnik Sen, Michelle Lacey, Carl Baribault, V K Chaithanya Ponnaluri, Pierre Olivier Esteve, Kenneth C Ehrlich, Mia Meletta, Sriharsa Pradhan, Melanie Ehrlich","doi":"10.1080/15592294.2025.2508251","DOIUrl":"10.1080/15592294.2025.2508251","url":null,"abstract":"<p><p>Epigenetic changes are implicated in development, repair, and physiology of postnatal skeletal muscle (SkM). We generated methylomes for human myoblasts (SkM progenitor cells) and determined myoblast differentially methylated regions (DMRs) for comparison to the epigenomics and transcriptomics of diverse cell types. Analyses were from global genomic and single-gene perspectives and included reporter gene assays. One atypical finding was the association of promoter-adjacent hypermethylation in myoblasts with transcription turn-on, but at downmodulated levels, for certain genes (<i>e.g</i>., <i>SIM2</i> and <i>TWIST1</i>). In contrast, brain-specific <i>OLIG2</i> was in repressed chromatin and silent in most cell types but linked to hypermethylated DMRs specifically in myoblasts. The <i>OLIG2</i>-linked DMRs might be needed because of the overlapping or nearby binding of myogenic differentiation protein 1 (MYOD). We found genome-wide overlap of DMRs with MYOD or CCCTC-binding factor (CTCF) binding sites in myoblasts that is consistent with the importance of MYOD, as well as CTCF, in organizing myoblast transcription-enhancing chromatin interactions. We also observed some gene upregulation correlated with a special association of regional DNA hypomethylation with H3K36me3, H3K27ac, and H3K4me1 enrichment. Our study highlights unusual relationships between epigenetics and gene expression that illustrate the interplay between DNA methylation and chromatin epigenetics in the regulation of transcription.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2508251"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12160609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265736","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":"Advancements in DNA methylation technologies and their application in cancer diagnosis.","authors":"Yang Yang, Xiaosha Wen, Li Wang","doi":"10.1080/15592294.2025.2539995","DOIUrl":"10.1080/15592294.2025.2539995","url":null,"abstract":"<p><p>DNA methylation is a common epigenetic modification that maintains the integrity of the DNA sequence while profoundly influencing gene expression and phenotypic variation. Aberrant DNA methylation has been associated with the onset and progression of diseases, including cancer, metabolic disorders, and neurodevelopmental disorders. Recent advancements in detection technology led to a gradual increase in the exploration of DNA methylation as a valuable biomarker for cancer diagnosis and therapy. Single-base resolution has been achieved for whole-genome methylation analyses through second-generation sequencing technology, significantly enhancing detection efficiency. Additionally, PCR-based methods offer simple and feasible solutions for methylation analysis. In this review, we discuss various methods for detecting DNA methylation, focusing on bisulfite conversion-based techniques, methylation-sensitive restriction enzyme methods, enzyme conversion-based methods, third-generation sequencing approaches, and artificial intelligence. Furthermore, we briefly summarize the methylation biomarkers used for tumor diagnosis and the corresponding sample types employed. We believe that this information provides valuable insights for selecting and optimizing DNA methylation analysis tools.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2539995"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144728902","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":"Correction.","authors":"","doi":"10.1080/15592294.2025.2554384","DOIUrl":"10.1080/15592294.2025.2554384","url":null,"abstract":"","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2554384"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12427433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145033041","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":"Tributyltin chloride alters the structural, genomic, and epigenomic integrity of postejaculatory mammalian sperm.","authors":"Muhammad S Siddique, Santosh Anand, Marie-Pierre L Gauthier, Jason O Brant, Michael P Kladde, Ramji K Bhandari, Bradford W Daigneault","doi":"10.1080/15592294.2025.2552129","DOIUrl":"10.1080/15592294.2025.2552129","url":null,"abstract":"<p><p>A global priority for ameliorating male factor infertility includes identification of environmental factors and mechanisms that impact sperm function. Detection of endocrine disrupting chemicals (EDC) in seminal plasma and within the female reproductive tract has created an urgent need to understand how environmental stressors alter postejaculatory sperm function. Tributyltin chloride (TBT) is an EDC and epigenetic modifier that causes reproductive disorders. The consequences of TBT exposure on postejaculatory sperm remain unknown. The present study was aimed at identifying structural, genomic, and epigenomic consequences of TBT exposure to postejaculatory sperm. Bovine sperm were exposed to TBT (0, 1, 10, 100 nM) for 24 h followed by quantification of sperm kinematics, DNA integrity, and methylation status. No differences were detected in sperm kinematics or capacitation status. However, acrosome integrity was compromised at both 0 and 24 h (<i>P</i> ≤ 0.05). Sperm DNA integrity was also negatively affected after 24 h. Whole-genome methyl-seq revealed ~750 differentially methylated regions (DMRs) associated with exposure to TBT. Ingenuity Pathway Analyses and Gene Ontology identified embryo development, cell signaling, and transcriptional regulation as the most relevant bio-functions of TBT altered DMRs. In conclusion, postejaculatory mammalian sperm exposure to TBT negatively affected parameters important for sperm function while altering DNA integrity and the methylation profile of gene promoter regions. Consequences of sperm exposure to TBT included cellular and molecular mechanisms that are important for sperm function but remain undetected by routine clinical analyses. These findings provide new insight into environmental impacts on postejaculatory sperm structure and function.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2552129"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12439583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063660","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":"Fumonisin B₁ induces global DNA hypermethylation in human glioblastoma U87MG cells.","authors":"Ashmika Foolchand, Terisha Ghazi, Anil A Chuturgoon","doi":"10.1080/15592294.2025.2523690","DOIUrl":"10.1080/15592294.2025.2523690","url":null,"abstract":"<p><p>Fumonisin B₁ (FB₁) is a common maize contaminant known to induce toxicity and carcinogenesis in humans and animals; however, its epigenetic mechanisms remain poorly understood. DNA methylation is an epigenetic modification that controls gene expression through DNA methyltransferase and demethylase activities. In this study, the effect of FB₁ on DNA methylation in brain glioblastoma U87MG cells was evaluated. FB₁ cytotoxicity was determined by the MTT assay and an IC₅₀ value of 880 µM FB₁ was obtained. The ELISA-based global DNA methylation assay displayed an increase in 5-methylcytosine levels. qPCR and western blot revealed a significant increase in DNA methyltransferase expressions (DNMT1, DNMT3A, and DNMT3B) and a significant decrease in demethylase expression (MBD2). This data indicates that FB₁ induces global DNA hypermethylation, through increased DNA methyltransferase expressions and DNA demethylase suppression in U87MG cells, thus suggesting an alternative mechanism of toxicity.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2523690"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203852/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144495357","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":"Refeeding with different levels of dietary carbohydrate modulates epigenetic stability through global DNA (de)methylation and histone modifications in juvenile and adult Nile tilapia (<i>Oreochromis niloticus</i>).","authors":"Sirijanya Thongchaitriwat, Suksan Kumkhong, Cécile Heraud, Karine Dias, Stephane Panserat, Surintorn Boonanuntanasarn, Lucie Marandel","doi":"10.1080/15592294.2025.2566514","DOIUrl":"10.1080/15592294.2025.2566514","url":null,"abstract":"<p><p>The Nile tilapia (<i>Oreochromis niloticus</i>) exhibits a strong metabolic response to dietary carbohydrates (CHO). Short-term refeeding after fasting with a high-carbohydrate (HC) diet has been shown to modulate CHO metabolism, but the role of epigenetic regulation in this response remains unclear. This study investigated how short-term refeeding with either a HC [639.2 g kg^-1 diet]/low-protein [164.9 g kg^-1 diet] (HC/LP) diet or a low-CHO [47.4 g kg^-1 diet]/high-protein [607.9 g kg^-1 diet] (LC/HP) diet influences global DNA methylation and demethylation, histone modifications, and mRNA levels of epigenetic regulators in the liver and muscle of juvenile and adult Nile tilapia. Following a 4-day fasting period, fish were refed for 4 days with either HC/LP or LC/HP diets. Compared to the fasted state, refeeding with either diet altered epigenetic markers by: (1) decreasing hepatic global DNA 5-mC oxidative derivatives-5-hmdC in juveniles, and both 5-hmdC and 5-cadC in adults; (2) inducing histone hypermethylation and/or hyperacetylation - H3K9ac (hepatic) and H3K36me3 (muscular) in juveniles, and H3K9me3 and H3K9ac (muscular) in adults; and (3) promoting expression of enzymes related to DNA hypermethylation (upregulated <i>dnmt</i>, downregulated <i>tet</i>) and histone hypermethylation/acetylation (upregulated <i>setd1b</i>, <i>kmt2, suv39h1b</i>; downregulated <i>kdm4, sirt5</i>). Diet-specific effects included hepatic H3K36 hypomethylation and H3K9 hypoacetylation in juveniles fed HC/LP, accompanied by upregulation of <i>kdm4b, kdm4c</i>, and <i>sirt5</i>. In adults, HC/LP refeeding induced muscular DNA hypomethylation and H3K9 hypoacetylation, associated with upregulation of <i>tet, sirt2</i>, and <i>sirt5</i>. Refeeding following fasting induced histone hypermethylation and/or hyperacetylation, while HC refeeding was particularly associated with muscular global DNA hypomethylation and histone hypoacetylation/methylation.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2566514"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12482430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184965","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":"Mechanism of crosstalk between DNA methylation and histone acetylation and related advances in diagnosis and treatment of premature ovarian failure.","authors":"Jing Li, Qianhui Liao, Yurou Guo, Jiaheng Zhang, Ruyi Zhang, Qiyu Liu, Huiping Liu","doi":"10.1080/15592294.2025.2528563","DOIUrl":"10.1080/15592294.2025.2528563","url":null,"abstract":"<p><p>Premature ovarian failure (POF) affects 1-3.5% of women under 40 years of age, characterized by irreversible depletion of the follicular pool and decline in oocyte quality, with its pathogenesis remaining incompletely understood. Current mainstream therapies, such as hormone replacement therapy, only alleviate symptoms, fail to reverse the underlying functional decline, and carry long-term risks, necessitating the exploration of novel strategies targeting the etiology. This review systematically dissects the central role of epigenetic regulation in POF. First, DNA methylation governs female reproductive lifespan by reprogramming the dormant-activation balance of primordial follicles and maintaining epigenetic memory in oocytes. Second, histone modification homeostasis determines ovarian endocrine function by influencing granulosa cell senescence and steroid hormone synthesis. Additionally, non-coding RNAs form regulatory hubs by constructing competing endogenous RNA networks that integrate oxidative stress and developmental signaling pathways. These mechanisms provide new insights into the pathological basis of POF, identify potential biomarkers, and offer a theoretical framework for deciphering targeted intervention strategies and developing precision epigenetic therapies to delay POF progression.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2528563"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239803/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575094","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":"Acetaldehyde-driven mRNA methylation and expression changes in ethanol-metabolizing enzyme genes.","authors":"Ji Sun Koo, Qiansheng Zhan, Huiping Zhang","doi":"10.1080/15592294.2025.2493865","DOIUrl":"https://doi.org/10.1080/15592294.2025.2493865","url":null,"abstract":"<p><p>This study examines how the alcohol metabolite acetaldehyde modulates mRNA methylation and expression of ethanol-metabolizing genes, uncovering its epigenetic role in ethanol metabolism. Using neuron-like (SH-SY5Y) and non-neuronal (SW620) cellular models, we examined the effects of chronic intermittent acetaldehyde (CIA) exposure and subsequent withdrawal (CIA+WD) on global RNA m6A modifications and the methylation and expression of three brain ethanol-metabolizing genes: <i>CAT</i> (catalase), <i>CYP2E1</i> (cytochrome P450 2E1), and <i>ALDH2</i> (aldehyde dehydrogenase 2). A 3-week CIA exposure, with or without 24-hour withdrawal, did not significantly alter global m6A methylation levels in either cell line. However, acetaldehyde exposure/withdrawal induced hypermethylation at the mRNA stop codon regions of <i>ALDH2</i> (CIA: <i>p</i> = 0.002; CIA+WD: <i>p</i> = 0.055) and <i>CAT</i> (CIA: <i>p</i> = 0.077; CIA+WD: <i>p</i> = 0.036) in SH-SY5Y cells, but not in SW620 cells. Furthermore, <i>ALDH2</i> mRNA expression was significantly upregulated in both cell types following exposure (SH-SY5Y: <i>p</i> = 0.073 [CIA] and 0.00002 [CIA+WD]; SW620: <i>p</i> = 0.0009 [CIA] and 0.00008 [CIA+WD]). In contrast, <i>CYP2E1</i> mRNA methylation and the expression of <i>CYP2E1</i> and <i>CAT</i> remained unchanged. These findings highlight the cell-specific epigenetic effects of acetaldehyde, particularly its role in modulating mRNA methylation and expression of <i>ALDH2</i>, a key enzyme in alcohol metabolism.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2493865"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12013419/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985662","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 SCARNA8 promotes atherosclerotic plaque instability by inhibiting macrophage efferocytosis.","authors":"Xiaoliang Yin, Xiaodong Chen, Tao Wang, Jianling Yang, Jiahui Yu, Jun Yang","doi":"10.1080/15592294.2025.2487317","DOIUrl":"10.1080/15592294.2025.2487317","url":null,"abstract":"<p><p>In recent years, findings suggest that long noncoding RNAs (lncRNAs) are closely related to the development of atherosclerosis (AS), but there is a lack of studies on the involvement of lncRNA-regulated cytosolic burial in the regulation of AS. In this study, we investigated the mechanism by which lncRNA SCARNA8 affects macrophage cell burial to regulate AS. The cytosolic burial-associated target gene regulated by lncRNA SCARNA8 was PPARG. LncRNA SCARNA8 was increased in the carotid unstable plaque group, whereas PPARG was decreased. Ox-LDL led to the up-regulation of lncRNA SCARNA8 expression and apoptosis in Raw264.7 cells in a time-, concentration-dependent manner. Knockdown of lncRNA SCARNA8 upregulated PPARG and reduced apoptosis in Raw264.7 cells. In addition, knockdown of lncRNA SCARNA8 improved the stability of atherosclerotic plaques by promoting cellular burial of Raw264.7 cells. LncRNA SCARNA8 is a key regulator of plaque vulnerability, and targeting lncRNA SCARNA8 May provide a novel means for the prevention and treatment of AS.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2487317"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12077458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143973896","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}