铜
新陈代谢
细胞凋亡
化学
程序性细胞死亡
细胞代谢
有机体
肿瘤进展
肿瘤微环境
细胞生物学
癌症研究
癌症
生物化学
肿瘤细胞
生物
遗传学
有机化学
作者
Wenyan Yu,Xinlin Hong,Guojuan Wang,Chen Zhong,Yuwei Yan,Qingqing Ma,Yijie Lai,Naicheng Zhu,Xiudan Chen,Nanxin Li,Jianfeng Weng
出处
期刊:Metallomics
[Oxford University Press]
日期:2025-07-17
标识
DOI:10.1093/mtomcs/mfaf025
摘要
Abstract Cancer is an intractable global public health problem. The p53 protein encoded by the TP53 is a tumor suppressor, but it is mutated in many tumors, which promotes the initiation and progression of tumors. The mechanisms of p53 regulates tumors are focused on regulating apoptosis, cell cycle arrest, nutrient metabolism, iron metabolism and redox levels. Copper is a necessary trace element and abnormal copper homeostasis not only damages the organism but also affects tumor progression. It has confirmed that p53 can bind to copper, respond to copper levels, and regulate copper metabolism. Some anti-tumor mechanisms of copper-related compounds are related to p53. Herein, we focus on reviewing how to regulate copper-binding proteins by p53, as well as its involvement in copper-mediated cell death and tumor drug resistance. It summarizes the pertinent mechanisms of wild-type p53 in regulating cancers via copper metabolism, which aiming to provide new ideas for future cancer therapy.
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