Targeting cuproplasia and cuproptosis in cancer.

Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101500077 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1759-4782 (Electronic) Linking ISSN: 17594774 NLM ISO Abbreviation: Nat Rev Clin Oncol Subsets: MEDLINE

Original Publication: London : Nature Pub. Group

Neoplasms*/drug therapy ; Neoplasms*/pathology ; Neoplasms*/genetics ; Neoplasms*/metabolism ; Copper*/metabolism; Humans ; Mitochondria/metabolism ; Mitochondria/drug effects

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.
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789U1901C5 (Copper)

Date Created: 20240315 Date Completed: 20240424 Latest Revision: 20240503

20240504

10.1038/s41571-024-00876-0

38486054