Cancers · 3 authors, 2 centres
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This narrative review synthesizes the mechanisms of copper-induced cell death (cuproptosis), focusing on how copper ionophores such as elesclomol and disulfiram elevate intracellular copper to trigger oxidative stress, disrupt mitochondrial respiration, and impair protein lipoylation. The authors identify cuproptosis as a potential avenue for cancer therapy while noting that regulatory mechanisms and clinical translation remain to be determined.
This narrative review surveys the biochemical mechanisms underlying cuproptosis, a recently identified form of cell death induced by imbalanced copper levels. The authors describe how copper ionophores, specifically elesclomol and disulfiram, increase intracellular copper levels, triggering oxidative stress and disrupting mitochondrial respiration and protein lipoylation, ultimately leading to cell death. The review discusses the role of copper transporters and potential biomarkers, as well as copper nanomaterials, ionophores, and chelators as therapeutic strategies in oncology. Physiological copper mechanisms are explored through Wilson and Menkes disease. The review identifies cuproptosis-related targets and biomarkers relevant to cancer therapy but notes that regulatory mechanisms underlying cuproptosis must first be determined before clinical progression. A key limitation is that this is a survey of existing literature without original experimental data, and the correlation between cuproptosis and cancer requires further exploration through clinical trials.
