长期长期暴露于甲和甲基醇诱导了肺癌细胞的多药性耐药性
Tongkuo Yuan1, Yu Zheng1, Jing Chen1
1Division of Life Sciences and Medicine, School of Biomedical Engineering (Suzhou), University of Science and Technology of China, Suzhou, Jiangsu, 215163, China; CAS Key Lab of Bio-Medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, Suzhou, Jiangsu, 215163, China.
Environmental pollution (Barking, Essex : 1987)
|February 15, 2025
概括
环境污染物如甲和甲基醇可以诱导肺癌细胞的多药性耐药性 (MDR),影响化疗的有效性. 这项研究揭示了一种独特的MDR机制,不涉及ABC载体,这对于了解环境癌症风险至关重要.
科学领域:
- 环境科学 环境科学
- 癌症生物学 癌症生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 长期暴露于环境污染物与癌症的发展和进展有关.
- 常见污染物对癌症治疗疗效的影响在很大程度上是未知的.
- 甲 (B[a]P) 和甲基醇 (CL) 是普遍存在的环境化合物.
研究的目的:
- 调查B[a]P和CL对肺癌 (A549) 细胞化疗疗效能的慢性影响.
- 确定这些污染物是否诱导化学抵抗,并了解潜在的机制.
- 探索ABC载体在污染物诱导的化学阻力中的作用.
主要方法:
- 对A549肺癌细胞暴露于B[a]P和CL.
- 对多克索鲁比 (DOX) 和西斯 (CDDP) 的化学抗药性评估.
- 分析ABC输送体表达和活动.
- 使用伤口愈合和亡试验评估亡,扩散和迁移途径.
主要成果:
- 对B[a]P和CL的重复暴露诱导了对DOX和CDDP的化学抵抗,形成了多重耐药 (MDR) 细胞.
- 与耐污染物细胞相比,抗污染物细胞的ABC转运体表达减少,但与耐DOX细胞相比,抗性增加.
- 耐污染物细胞表现出反亡,增殖和迁移通路的增强上调.
结论:
- 像B[a]P和CL这样的非基板环境污染物可以在肺癌细胞中诱导一种独特的MDR机制.
- 这种机制涉及调节亡,增殖和迁移的途径,独立于典型的ABC载体活动.
- 这些发现对于评估污染物对癌症患者治疗结果的环境风险至关重要.
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