STIM1 N-链接的糖化促进诱导的恶性表型通过激活 SOCE 在膀上皮细胞
Pinya Liu1, Lei Zhang2, Qing Zhou3
1Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention, Ministry of Education (China Medical University), Shenyang, Liaoning Province, 110122, China; The Key Laboratory of Liaoning Province on Toxic and Biological Effects of Arsenic, China Medical University, Shenyang, Liaoning Province, 110122, China; School of Public Health, Dalian Medical University, Dalian, Liaoning Province, 116044, China.
Chemico-biological interactions
|December 10, 2025
概括
长时间暴露于会通过破坏 (Ca2+) 恒温来增加膀癌的风险. 这项研究确定STIM1介导的储存运行的进入是诱导尿细胞转化的关键机制.
科学领域:
- 环境健康 环境健康
- 癌症生物学 癌症生物学
- 细胞生理学 细胞生理学
背景情况:
- 流行病学研究将无机暴露与增加膀癌风险联系起来.
- 这种关联背后的精确分子机制在很大程度上是未知的.
- 离子 (Ca2+) 是细胞过程的关键调节者,它们的失调有助于恶性瘤.
研究的目的:
- 为了研究平衡在诱导的膀癌中的作用.
- 阐明涉及对尿细胞致癌作用的特定细胞通路.
主要方法:
- 在试验室中,人类膀上皮细胞 (SV-HUC-1) 暴露于甲 (NaAsO2).
- 在体内处理C57BL/6小鼠,在饮用水中使用不同度的NaAsO2.
- 分析水平,细胞增殖,干细胞,上皮细胞-介质细胞过渡 (EMT) 和STIM1/ORAI1相互作用.
主要成果:
- 长期暴露于使SV-HUC-1细胞中的细胞内Ca2+水平升高.
- 治疗增强了细胞增殖,干性和EMT.
- 由STIM1和ORAI1介导的储存运行的入 (SOCE) 对于诱导的Ca2+失调和细胞转化至关重要.
- 在N131的STIM1N相关的糖化对其功能至关重要.
结论:
- 平衡失衡是诱导的膀癌发病和进展的一个重要机制.
- STIM1介导的SOCE在对尿细胞的致癌作用中发挥着关键作用.
- 向STIM1或信号通路可能为与有关的膀癌提供治疗策略.
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