通过PI3K/AKT/NF-κB介导的EMT促进肺腺癌细胞的增殖
Ruijian Liu1, Qiuyu Yang1, Shanshan Fan1
1Guangdong Provincial Emergency Hospital, The Affiliated Guangdong Second Provincial General Hospital of Jinan University, 466 Middle Xingang Road, Guangzhou, 510317, Guangdong, People's Republic of China.
概括
像PFOS这样的 perfluoroalkyl物质通过抑制细胞亡和增强迁移来促进肺癌细胞的生长. 这项研究显示,PFOS激活PI3K/ AKT/ NF- kB通路,导致肺腺癌的发展.
科学领域:
- 环境健康
- 毒理学
- 癌症学
背景情况:
- 甲基和多甲基物质 (PFAS) 是广泛使用的合成化学物质.
- 甲硫酸 (PFOS) 暴露与健康问题有关,但其在肺癌中的作用尚不清楚.
研究的目的:
- 研究PFOS对肺腺癌 (LUAD) 细胞系的影响.
- 阐明LUAD中的PFOS致癌机制.
主要方法:
- 在H1299和A549LUAD细胞中评估了PFOS诱导的增殖,抗亡性质和上皮介质转变 (EMT).
- 研究PI3K/AKT/NF-κB通路的激活及其在亡抑制中的作用.
主要成果:
- 通过抑制细胞灭亡,PFOS显著促进了LUAD细胞的生长.
- 酸加速了EMT, 增强了细胞迁移.
- PFOS激活了PI3K/AKT/NF-κB通路,促进了它们的增殖和迁移.
结论:
- 暴露于PFOS可能会加剧肺部疾病或诱导致癌.
- PFOS抑制了亡并激活了LUAD中的PI3K/ AKT/ NF- kB信号.
- 这些发现提供了PFOS在肺腺癌中致癌潜力的证据.
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