促进ROS介导的支气管上皮细胞的恶性转变,通过专门降低TXNL1表达的调节
Lingling Zhao1, Xueli Jiao2,3, Hongyan Li2
1Zhejiang Provincial Key Laboratory of Medical Genetics, Key Laboratory of Laboratory Medicine, Ministry of Education, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China. zhaolingling@wmu.edu.cn.
Communications biology
|November 22, 2025
概括
暴露会通过影响USP10和DNMT1来降低类型1 (TXNL1),增加肺癌风险. 恢复TXNL1可能会预防引起的癌症.
科学领域:
- 环境健康 环境健康
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 暴露是一种已知的肺癌原体,与活性氧物种 (ROS) 和DNA损伤有关.
- 对ROS水平的影响的确切机制尚未完全理解.
研究的目的:
- 阐明样氧素1 (TXNL1) 在诱导的肺癌发生中的作用.
- 研究通过哪些分子途径影响TXNL1表达和氧化还原稳定.
主要方法:
- 在体外和体内研究来评估TXNL1的表达.
- 研究TXNL1增强对诱导的细胞变化的影响.
- 分析USP10和DNMT1在对TXNL1.1的影响中的作用.
主要成果:
- 降低了TXNL1的表达,与其他ROS清理基因相反.
- 增加的TXNL1抑制了引起的ROS,DNA损伤和恶性转变.
- 降低了USP10的调节,导致TXNL1的降解,并提高了DNMT1的调节,导致USP10促进剂高甲基化.
结论:
- 通过DNMT1-USP10-TXNL1通路破坏了氧化还原稳态.
- 这一途径代表了预防引起的肺癌的潜在治疗标.
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