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来自泰国北部的生物质雾PM2.5驱动基因型特定的氧化应激和非小细胞肺癌细胞的转录基因重塑
Sakawwarin Prommana1, Sitthisak Intarasit1,2, Saruda Thongyim2,3
1Department of Biology, Faculty of Science, Chiang Mai University, Chiang Mai 50200, Thailand.
Toxics
|January 28, 2026
概括
生物质烟雾细颗粒物 (PM2.5) 导致基因型特定的氧化应激,并改变非小细胞肺癌 (NSCLC) 细胞中的基因表达,影响瘤进展途径.
科学领域:
- 环境科学 环境科学
- 分子生物学分子生物学
- 在瘤学瘤学.
背景情况:
- 来自生物质烟雾的细颗粒物 (PM2.5) 在东南亚普遍存在.
- 这种特定的PM2.5对遗传多样性非小细胞肺癌 (NSCLC) 细胞的影响尚不清楚.
研究的目的:
- 调查清迈雾衍生的PM2.5对三种不同的NSCLC细胞系中氧化应激和基因表达的影响.
- 为了确定肺癌细胞中急性PM2.5暴露的基因型特异反应.
主要方法:
- 暴露A549 (KRAS突变型),NCI-H1975 (EGFR突变型) 和NCI-H460 (KRAS/PIK3CA突变型) NSCLC细胞在PM2.5.5的不同度下.
- 评估细胞活力 (MTT),反应性氧物种 (ROS),甲 (MDA),线粒体光和全转录组测序 (RNA-seq).
主要成果:
- 暴露于PM2.5诱导了剂量和时间依赖的活力丧失,细胞系之间的敏感性差异.
- 观察到基因型特定的氧化应激模式,包括A549的累积增加和NCI-H1975的可逆峰值.
- RNA-seq揭示了与异生菌代谢,氧化应激和瘤进展相关的基因的显著变化,氧化应激和免疫信号的途径得到丰富.
结论:
- 生物质雾衍生的PM2.5通过诱导基因型依赖的氧化应激显著影响NSCLC细胞.
- 暴露于PM2.5触发了转录重编程,影响了参与癌症进展和免疫反应的关键途径.
- 这些发现凸显了生物质烟雾PM2.5在遗传多样性人群中肺癌发展和进展中的潜在风险.
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