The relationship between copper metabolism and p53 activity in tumors.

IF 2.9 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Metallomics Pub Date : 2025-08-05 DOI:10.1093/mtomcs/mfaf025
Wenyan Yu, Xinlin Hong, Guojuan Wang, Chen Zhong, Yuwei Yan, Qingqing Ma, Yujuan Lai, Naicheng Zhu, Xiudan Chen, Nanxin Li, Jianfeng Weng
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引用次数: 0

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.

肿瘤中铜代谢与p53活性的关系。
癌症是一个棘手的全球公共卫生问题。TP53编码的p53蛋白是一种肿瘤抑制因子,但在许多肿瘤中发生突变,促进肿瘤的发生和发展。p53调控肿瘤的机制主要集中在调控细胞凋亡、细胞周期阻滞、营养代谢、铁代谢和氧化还原水平。铜是人体必需的微量元素,铜稳态异常不仅会损害机体,还会影响肿瘤的发展。已经证实p53可以与铜结合,对铜水平作出反应,调节铜的代谢。一些铜相关化合物的抗肿瘤机制与p53有关。本文就p53如何调控铜结合蛋白及其在铜介导的细胞死亡和肿瘤耐药中的作用进行综述。本文综述了野生型p53通过铜代谢调控癌症的相关机制,旨在为未来的癌症治疗提供新的思路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Metallomics
Metallomics 生物-生化与分子生物学
CiteScore
7.00
自引率
5.90%
发文量
87
审稿时长
1 months
期刊介绍: Global approaches to metals in the biosciences
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