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在与MASLD相关的肝细胞癌中,p53通过调节线粒体中pyruvate载体来调节葡萄糖代谢重编程

Ze Wang¹, Fei Tian², Yiming Wang¹

¹Department of Hepatobiliary Surgery, Kailuan General Hospital Affiliated North China University of Science and Technology, 57 Xinhua East Road, Lubei District, Tangshan, 063000, China.

Hepatology international

|October 25, 2025

概括

通过PUMA-MPC通路改变葡萄糖代谢,p53促进了代谢功能障碍相关的脂肪性肝病 (MASLD) 的肝细胞癌 (HCC). 这突显了p53在代谢压力下具有促瘤作用.

科学领域:

肝病学和瘤学肝病学和瘤学
分子生物学分子生物学
代谢研究的研究.

背景情况:

与代谢功能障碍相关的脂肪性肝病 (MASLD) 是肝细胞癌 (HCC) 的一个不断增长的原因.
代谢重编程和MASLD-HCC之间的分子联系尚未完全理解.
在MASLD-HCC进展中p53的作用需要进一步阐明.

研究的目的:

通过线粒体的pyruvate载体 (MPC) 轴研究p53在调节葡萄糖代谢中的作用.
确定p53-MPC轴对MASLD-HCC进展的影响.
在这个途径中探索潜在的治疗点.

主要方法:

已建立的MASLD-HCC小鼠和细胞模型.
使用药理和遗传工具调节p53活性和表达.
使用抑制剂和过度表达等离子体,研究了MPC通路功能.
通过Western blot,qPCR,CCK-8,Oil Red O染色和功能分析分析了分子和细胞变化.

主要成果:

在MASLD到HCC进展过程中,p53表达被上调.
通过p53-PUMA-MPC轴,p53促进糖解并抑制葡萄糖生成.
通过p53降低MPC的调节驱动了代谢重编程,脂质积累和瘤细胞迁移.
对MPC的调节逆转了p53诱导的瘤进展的影响.

结论:

在MASLD-HCC中,TP53驱动了通过PUMA-MPC轴的代谢重编程和糖解依赖的进展.
在代谢压力下,p53表现出上下文依赖的前瘤功能,挑战其传统的瘤抑制作用.
在MASLD-HCC中,p53-PUMA-MPC通路是精密治疗的潜在目标.

关键词:

葡萄糖代谢重编程葡萄糖代谢重编程肝细胞癌是肝细胞癌.代谢功能障碍相关的脂肪性肝病线粒体中的pyruvate载体.在 p53 里,p53 是一个 p53 号码.

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