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长期低剂量暴露对人类肝细胞中DNA甲基化和基因表达的影响

Sandra Stößer¹, Tatjana Lumpp¹, Franziska Fischer¹

¹Department of Food Chemistry and Toxicology, Institute of Applied Biosciences (IAB), Karlsruhe Institute of Technology (KIT), 76131 Karlsruhe, Germany.

International journal of molecular sciences

|October 28, 2023

概括

慢性低剂量暴露会导致肝细胞中的全球DNA低甲基化. 这种表观遗传变化可能会导致诱导的致癌性,潜在的机制涉及蛋白质相互作用,而不是直接的基因下调.

科学领域:

环境毒理学环境毒理学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
癌症研究癌症研究

背景情况:

暴露是与癌症和其他疾病相关的全球健康问题.
表观遗传修饰,如DNA甲基化变化,与的致癌性有关.
化物诱导的DNA甲基化变化的机制尚不清楚.

研究的目的:

为了研究慢性低剂量化暴露对人类肝细胞中DNA甲基化的影响.
探索与DNA甲基化和细胞过程相关的对基因表达的影响.

主要方法:

人类HepG2肝癌细胞在短期 (24小时) 和长期 (10,20天) 期间用甲 (0.5-10μM) 治疗.
分析了全球DNA甲基化,细胞周期分布和基因表达.
量化了DNA甲基转移酶基因 (DNMT1,DNMT3A,DNMT3B) 的表达.

主要成果:

短期暴露对DNA甲基化没有影响.
长期暴露在化物中导致全球DNA低甲基化.
诱导了DNA甲基转移酶基因DNMT1和DNMT3B,而DNMT3A则被下调.
参与DNA损伤,炎症,氧化应激和金属稳态的基因受到时间和度依赖的方式的影响.

结论:

慢性低剂量化物暴露会在肝细胞中诱导全球DNA低甲基化.
观察到的低甲基化并不能通过对DNA甲基转移酶基因的持续下调来解释.
蛋白级相互作用可能是亚石表观遗传效应的关键机制.

关键词:

在DNA甲基转移酶中.这是一种HepG2型肝炎.亚是一种.细胞循环中的细胞循环.细胞毒性细胞毒性基因表达特征基因表达特征低甲基化低甲基化.

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