Copper is an essential element for sustaining life. However, disruptions in copper homeostasis underpin disease, as illustrated by cuproptosis, an emerging form of cell death resulting from aberrant a...

Yang et al. report that HIF-1α acts as a main driver of tumor resistance to cuproptosis under hypoxia. Mechanistically, they reveal that HIF-1α can repress DLAT expression and promote MT2A to sequeste...

Lei et al. reveal that radiotherapy (RT) elevates mitochondrial copper and induces cuproptosis by upregulating CTR1 and depleting mitochondrial glutathione. Furthermore, BACH1 downregulation confers radioresistance by upregulating MT1E/X-mediated cuproptosis defense. Correspondingly, copper-loaded copper ionophores restore RT sensitivity by enhancing cuproptosis, highlighting a therapeutic strategy to overcome tumor radioresistance.

Lei et al. reveal that radiotherapy (RT) elevates mitochondrial copper and induces cuproptosis by upregulating CTR1 and depleting mitochondrial glutathione. Furthermore, BACH1 downregulation confers r...

Reduced levels of the essential metabolite heme are a common feature of acute myeloid leukemia, and consequently, leukemic cells are highly sensitive to inhibition of de novo heme synthesis. Blockade ...

Jiang et al. review the metabolic foundations of cuproptosis, a copper-driven form of regulated cell death linked to mitochondrial metabolism. They discuss how copper homeostasis, lipoylation, and redox pathways control cuproptosis and highlight emerging therapeutic opportunities to exploit this metabolic vulnerability in cancer and other diseases.

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Cuproptosis is a recently defined form of regulated cell death (RCD) driven by copper-induced mitochondrial proteotoxic stress. Distinct from other RC…

Read the full paper: FDX1 expression promotes DSF/Cu-induced cuproptosis in gastric cancer cells

Read the full paper: PRMT5‐Dependent Stabilization of VPS34 Orchestrates Copper Trafficking to Shield Cancer Cells from Cuproptosis and Radiotherapy

Recently, a copper-dependent form of cell death called cuproptosis has been described, distinct from apoptosis, ferroptosis, and other known pathways. Cuproptosis is defined by excessive copper binding to lipoylated proteins, causing their aggregation and leading to cell death. Here, we discuss recent advances in understanding cuproptosis, focusing on its molecular mechanisms, physiological regulators, and therapeutic potential in cancer.

Copper binding drives MYH9 polymerization, triggering cytoskeletal collapse and cuproptosis. HThPA releases intracellular copper through glutathione depletion, exposing a therapeutic vulnerability in drug-resistant tumors.

Cell Death & Differentiation - Cuproptosis: an emerging member of the immunogenic cell death family