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双S通过调节WNT5A依赖的EMT通路来促进清细胞细胞癌的进展
Hua Zhang1, Fei Lin1, Bo-Han Lin1
1Department of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China; Department of Urology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou 350212, China.
Toxicology
|March 14, 2025
概括
双S (BPS) 暴露增强细胞癌 (RCC) 细胞迁移和入侵,通过诱导上皮细胞-介质细胞过渡 (EMT). 向WNT5A可以抑制BPS诱导的RCC进展,提供潜在的治疗策略.
科学领域:
- 环境健康 环境健康
- 在瘤学瘤学.
- 分子生物学分子生物学
背景情况:
- 双S (BPS) 是一种常见的工业化学物质,具有已知的内分泌干扰特性.
- 虽然BPS与各种癌症有关,但其在细胞癌 (RCC) 发展中的具体作用尚不清楚.
研究的目的:
- 调查BPS影响RCC进展的机制.
- 为了确定关键的基因和途径参与BPS介导癌的发展.
主要方法:
- 细胞增殖,迁移和入侵试验 (CCK-8,scratch,Transwell) 在HK-2和786-O细胞上进行.
- 拉索回归确定了候选基因,功能分析阐明了它们的作用.
- 评估了表皮层-介质细胞过渡 (EMT) 标志物,并进行了WNT5A敲击.
主要成果:
- 0-10μM的BPS暴露不会影响细胞增殖,但显著增加了迁移和入侵.
- 在细胞中,BPS诱导了表皮层-介质酶过渡 (EMT).
- 确定了9个关键基因;WNT5A表达与BPS度相关,并调解了BPS诱导的迁移和EMT.
结论:
- BPS通过WNT5A依赖的EMT促进细胞迁移和入侵.
- 抑制WNT5A可以抑制BPS诱导的RCC进展.
- 这项研究揭示了BPS作为RCC的潜在驱动因素和WNT5A作为治疗点.
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