Ashmika Foolchand, Terisha Ghazi, Anil A Chuturgoon
{"title":"伏马菌素B1诱导人胶质母细胞瘤U87MG细胞整体DNA超甲基化。","authors":"Ashmika Foolchand, Terisha Ghazi, Anil A Chuturgoon","doi":"10.1080/15592294.2025.2523690","DOIUrl":null,"url":null,"abstract":"<p><p>Fumonisin B<sub>1</sub> (FB<sub>1</sub>) 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 FB<sub>1</sub> on DNA methylation in brain glioblastoma U87MG cells was evaluated. FB<sub>1</sub> cytotoxicity was determined by the MTT assay and an IC<sub>50</sub> value of 880 µM FB<sub>1</sub> 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 FB<sub>1</sub> 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":3.2000,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203852/pdf/","citationCount":"0","resultStr":"{\"title\":\"Fumonisin B<sub>1</sub> induces global DNA hypermethylation in human glioblastoma U87MG cells.\",\"authors\":\"Ashmika Foolchand, Terisha Ghazi, Anil A Chuturgoon\",\"doi\":\"10.1080/15592294.2025.2523690\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Fumonisin B<sub>1</sub> (FB<sub>1</sub>) 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 FB<sub>1</sub> on DNA methylation in brain glioblastoma U87MG cells was evaluated. FB<sub>1</sub> cytotoxicity was determined by the MTT assay and an IC<sub>50</sub> value of 880 µM FB<sub>1</sub> 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 FB<sub>1</sub> 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\":3.2000,\"publicationDate\":\"2025-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203852/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Epigenetics\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1080/15592294.2025.2523690\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/6/26 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Epigenetics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/15592294.2025.2523690","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/6/26 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Fumonisin B1 induces global DNA hypermethylation in human glioblastoma U87MG cells.
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.
期刊介绍：
Epigenetics publishes peer-reviewed original research and review articles that provide an unprecedented forum where epigenetic mechanisms and their role in diverse biological processes can be revealed, shared, and discussed.
Epigenetics research studies heritable changes in gene expression caused by mechanisms others than the modification of the DNA sequence. Epigenetics therefore plays critical roles in a variety of biological systems, diseases, and disciplines. Topics of interest include (but are not limited to):
DNA methylation
Nucleosome positioning and modification
Gene silencing
Imprinting
Nuclear reprogramming
Chromatin remodeling
Non-coding RNA
Non-histone chromosomal elements
Dosage compensation
Nuclear organization
Epigenetic therapy and diagnostics
Nutrition and environmental epigenetics
Cancer epigenetics
Neuroepigenetics
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