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通过调节miR-497-5p/TCF3轴,circPVT1促进了二氧化诱导的上皮层-介质细胞过渡
Siyun Zhou1, Yan Li2, Wenqing Sun1
1Department of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, China.
Journal of biomedical research
|March 26, 2024
概括
循环RNA PVT1 (circPVT1) 在肺细胞中促进二氧化诱导的上皮层-介质细胞过渡 (EMT). 准circPVT1/miR-497-5p/TCF3通路可能为肺纤维化提供新的治疗方法.
科学领域:
- 肺部医学 肺部医学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 表皮-介质细胞过渡 (EMT) 是二氧化诱导的肺纤维化的一个关键过程.
- 在这个过程中,循环RNAs (circRNAs) 的作用尚不清楚.
研究的目的:
- 为了研究circPVT1在诱导的EMT中的功能.
- 为了阐明底层的分子机制.
主要方法:
- 用细胞测试来评估EMT和细胞迁移.
- 细胞质和核分离试验确定了circPVT1的定位.
- 通过RNA免疫沉和拉下测定,确定了结合相互作用.
- 在处理的肺上皮细胞中分析了MiR-497-5p和TCF3的相互作用.
主要成果:
- 升高的circPVT1表达促进了EMT,并在处理的细胞中增强了细胞迁移.
- circPVT1主要局部在细胞质中,并与miR-497-5p结合.
- miR-497-5p通过向TCF3,一种抑制E-cadherin转录的抑制剂来抑制化物诱导的EMT.
- 肺上皮细胞中发现了circPVT1/miR-497-5p/TCF3轴,这些肺上皮细胞接受了诱导的EMT.
结论:
- circPVT1在促进二氧化诱导的EMT方面发挥着重要作用.
- 环PVT1/miR-497-5p/TCF3通路是一种参与肺上皮细胞对二氧化反应的新型机制.
- 这一途径为肺纤维化提供了潜在的治疗点.
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