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作者：SCI天天读
SCI
31 March 2024
Targeting cuproplasia and cuproptosis in cancer
(Nature Reviews Clinical Oncology, IF: 78.80)
Daolin Tang, Guido Kroemer & Rui Kang
CORRESPONDENCE TO: daolin.tang@utsouthwestern.edu; kroemer@orange.fr;rui.kang@utsouthwestern.edu
Abstract 摘要
Copper, an essential trace element that exists in oxidized and reduced forms, has pivotal roles in a variety of biological processes, including redox chemistry, enzymatic reactions, mitochondrial respiration, iron metabolism, autophagy and immune modulation; maintaining copper homeostasis is crucial as both its deficiency and its excess are deleterious. Dysregulated copper metabolism has a dual role in tumorigenesis and cancer therapy. Specifically, cuproplasia describes copper-dependent cell growth and proliferation, including hyperplasia, metaplasia and neoplasia, whereas cuproptosis refers to a mitochondrial pathway of cell death triggered by excessive copper exposure and subsequent proteotoxic stress (although complex interactions between cuproptosis and other cell death mechanisms, such as ferroptosis, are likely and remain enigmatic). In this Review, we summarize advances in our understanding of copper metabolism, the molecular machineries underlying cuproplasia and cuproptosis, and their potential targeting for cancer therapy. These new findings advance the rapidly expanding field of translational cancer research focused on metal compounds.
铜是一种必需的微量元素，以氧化和还原形式存在，对多种生物过程起着关键作用，包括氧化还原化学、酶促反应、线粒体呼吸、铁代谢、自噬和免疫调节；维持铜的稳态至关重要，是因为铜的缺乏和过量都是有害的。失调的铜代谢在肿瘤发生和癌症治疗中具有双重作用。具体来说，铜增生描述的是铜依赖性细胞生长和增殖，包括增生、异型增生和肿瘤，而铜死亡指的是由过量铜暴露和随后的蛋白质毒性应激触发的线粒体细胞死亡途径（尽管铜死亡与其他细胞死亡机制如铁死亡机制之间的复杂相互作用可能存在且仍然是个谜）。在这篇综述中，我们总结了关于铜代谢的理解进展、铜增生和铜死亡背后的分子机制，以及它们在癌症治疗中的潜在靶向。这些新发现推动了以金属化合物为重点的转化癌症研究领域的快速发展。
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