卵巢癌是一种致命性的妇科肿瘤，给全球各国带来巨大的经济压力。其频繁复发的严峻挑战需要探索新型细胞毒性药物、副作用最小的有效抗肿瘤药物以及克服对主要化疗药物耐药性的策略。这些努力旨在补充现有的药理学干预措施并阐明诱导细胞毒性的分子机制，这与传统的治疗方式不同。最近的科学研究揭示了一种新的细胞死亡形式，称为铜死亡，它取决于细胞内铜的浓度。与传统的细胞死亡机制不同，铜死亡表现出对线粒体呼吸的明显依赖，特别是三羧酸（TCA）循环。与正常细胞相比，肿瘤细胞表现出独特的代谢特征和升高的铜水平。铜死亡的出现为癌症治疗领域的靶向治疗干预提供了诱人的可能性。因此，本综述的主要目的是概述与铜诱导的细胞死亡相关的蛋白质和复杂机制，同时提供有关卵巢癌潜在治疗方法的知识的全面总结。这些发现将为促进卵巢癌定制治疗干预措施的进步提供有价值的参考。版权所有 © 2024 Elsevier Inc. 保留所有权利。

Ovarian cancer, a profoundly fatal gynecologic neoplasm, exerts a substantial economic strain on nations globally. The formidable challenge of its frequent relapse necessitates the exploration of novel cytotoxic agents, efficacious antineoplastic medications with minimal adverse effects, and strategies to surmount resistance to primary chemotherapeutic agents. These endeavors aim to supplement extant pharmacological interventions and elucidate molecular mechanisms underlying induced cytotoxicity, distinct from conventional therapeutic modalities. Recent scientific research has unveiled a novel form of cellular demise, known as copper-death, which is contingent upon the intracellular concentration of copper. Diverging from conventional mechanisms of cellular demise, copper-death exhibits a pronounced reliance on mitochondrial respiration, particularly the tricarboxylic acid (TCA) cycle. Tumor cells manifest distinctive metabolic profiles and elevated copper levels in comparison to their normal counterparts. The advent of copper-death presents alluring possibilities for targeted therapeutic interventions within the realm of cancer treatment. Hence, the primary objective of this review is to present an overview of the proteins and intricate mechanisms associated with copper-induced cell death, while providing a comprehensive summary of the knowledge acquired regarding potential therapeutic approaches for ovarian cancer. These findings will serve as valuable references to facilitate the advancement of customized therapeutic interventions for ovarian cancer.Copyright © 2024 Elsevier Inc. All rights reserved.