通过调节ROS介导的编程细胞死亡,NOX1抑制使HCC细胞对sorafenib和放射治疗敏感
Wei Mu1, Ya-Ge Shi1, Yu-Lun Jian1
1School of Public Health, Center for Single-Cell Omics, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Acta pharmacologica Sinica
|August 8, 2025
概括
尼古丁胺胺氨基二核酸氧化酶1 (NOX1) 驱动肝细胞癌 (HCC) 的进展和转移. 抑制NOX1可以减少瘤的扩散,并增强对索拉费尼布和放射治疗的敏感性,为HCC提供了一个有前途的治疗策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 肝细胞癌 (HCC) 的进展包括反应性氧物种 (ROS) 诱导的损伤和炎症.
- 尼古丁胺胺二核酸氧化酶 (NOXs) 调节ROS,但NOX1在HCC中的作用尚不清楚.
研究的目的:
- 研究NOX1在HCC进展,转移和治疗反应中的作用.
- 探索NOX1作为HCC的潜在治疗点.
主要方法:
- 对公共数据库和临床HCC标本的分析.
- 在实验室中使用NOX1敲击和ML171抑制的研究.
- 在体内转移和肝损伤的小鼠模型.
- 使用NOX1抑制剂,索拉芬尼和放射治疗的联合治疗.
主要成果:
- 在转移性HCC中NOX1表达升高与预后不佳相关.
- NOX1 抑制降低了 ROS,抑制了 HCC 细胞的移动性和侵入性,并减弱了转移.
- 联合NOX1抑制与索拉费尼布或放射疗法协同增强治疗疗效.
- 在HCC中,NOX1调节ROS稳态,抗氧化系统和炎症途径.
结论:
- NOX1对HCC进展,转移和治疗耐药性至关重要.
- 抑制NOX1是一种有前途的策略,可以改善HCC治疗结果.
- 向NOX1可以克服HCC患者对索拉费尼布和放射治疗的耐药性.
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