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向MED23通过抑制补偿增殖和促进ROS介导的细胞死亡来抑制肝细胞癌的发展

Xiaying Zhao¹, Zhichao Wang¹, Lihua Min²

¹State Key Laboratory of Genetics and Development of Complex Phenotypes, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438, China.

Cell death & disease

|December 23, 2025

概括

介导子单元MED23对于肝细胞癌 (HCC) 的发展至关重要. 抑制MED23稳定了NQO1,降低了ROS,并阻止了小鼠模型中的HCC进展,提供了一个新的治疗点.

科学领域:

肝细胞癌 (HCC) 研究研究
肝癌的分子机制肝癌的分子机制
调解者复杂的功能中介者的复杂功能.

背景情况:

肝细胞癌 (HCC) 与受损肝脏中的肝细胞增殖有关.
调解者复合体调节生理和病理过程中的转录因子和辅因子.
驱动HCC进展的分子机制在很大程度上是未知的.

研究的目的:

调查调解子单元MED23在肝细胞癌 (HCC) 发展中的作用.
阐明MED23影响HCC进展的分子机制.
确定针对MED23途径的HCC潜在的治疗策略.

主要方法:

使用二甲基胺 (DEN) 诱导的HCC小鼠模型.
进行了肝脏特异性Med23切除 (构成性和诱导性).
评估了肝细胞活力,NQO1蛋白稳定性,反应性氧物种 (ROS) 生产和IGF2表达.

主要成果:

在小鼠模型中,Med23的肝脏特异性切除显著抑制了HCC的发展.
通过降低NQO1稳定性和增加ROS,MED23缺陷降低了肝细胞活力.
MED23与RFX5合作调节IGF2增强剂功能,影响肝细胞活力和HCC.
在MED23缺乏细胞中的IGF2过度表达部分恢复了细胞生长并减少了细胞亡.

结论:

在HCC进展中,MED23-IGF2-NQO1轴具有重要意义.
在维持肝细胞活力和驱动HCC方面,MED23起着至关重要的作用.
准MED23-IGF2-NQO1通路为HCC提供了一个新的治疗策略.

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