雌激醇和[a]二烯的同时暴露有助于肺癌细胞A549通过AHR/AKT/ERK1/2途径扩散
Gaigai Huang1, Hao Feng2, Yu Zhou1
1Department of Clinical Laboratory, The First People's Hospital of Shuangliu District, Chengdu, China.
Annals of clinical and laboratory science
|January 5, 2024
概括
雌激素 (E2) 增强子[a]烯 (Bap) 对肺癌细胞的影响,促进细胞增殖和抑制细胞亡. 这涉及酸受体 (AHR) /AKT/ERK1/2通路,这表明雌激素在与烟草有关的肺腺癌中发挥了作用.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 环境健康 环境健康
背景情况:
- 雌激素在烟草引起的肺癌中的作用尚不清楚,对致癌物质混合物效应的理解有限.
- 研究往往侧重于单个因素,忽视了诸如雌激素和环境致癌物等综合影响.
研究的目的:
- 为了研究17β-雌二醇 (E2) 对[a]烯 (Bap) 诱导的肺癌细胞增殖的作用.
- 阐明在肺腺癌中雌激素和Bap之间相互作用的分子机制.
主要方法:
- 使用A549肺癌细胞的体外模型.
- 评估了E2和Bap对细胞增殖,细胞亡和关键蛋白质表达的单独和组合的影响.
- 研究了基碳化合物受体 (AHR) /AKT/ERK1/2信号通路的作用.
主要成果:
- 从肺腺癌患者的血清中发现E2的水平略高.
- Bap暴露增加了A549细胞的增殖,殖民地形成和PCNA和Bcl-2的表达,同时抑制了亡.
- E2增强了Bap的作用,通过AHR/AKT/ERK1/2通路促进了扩散和抗亡活性.
结论:
- 雌激素 (E2) 促进本佐[a]皮林 (Bap) 对肺癌细胞的增殖和抗亡作用.
- AHR/AKT/ERK1/2信号通路与E2增强Bap致癌作用的机制有关.
- 研究结果表明,雌激素在与烟草有关的肺癌发生过程中具有潜在的协同作用.
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