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Heme, copper, and a new way to kill cancer cells
Xi Zhao1, Li Zhuang1, Boyi Gan1
1Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Abstract:
Heme homeostasis influences mitochondrial metabolism and leukemia stem cell biology in acute myeloid leukemia. Lewis et al. uncover a surprising metabolic vulnerability in acute myeloid leukemia: suppression of heme biosynthesis primes leukemic cells for cuproptosis, a form of copper-dependent cell death. By linking heme depletion to mitochondrial cytochrome c oxidase (Complex IV) dysfunction, copper accumulation, and cuproptosis, the study integrates transcriptional regulation, mitochondrial metabolism, and metal homeostasis into a unified framework for selective cancer cell killing.
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