Research ArticleCancer

The mitophagy effector FUNDC1 controls mitochondrial reprogramming and cellular plasticity in cancer cells

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Science Signaling  28 Jul 2020:
Vol. 13, Issue 642, eaaz8240
DOI: 10.1126/scisignal.aaz8240

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Suppressing metastasis for proliferation

Cancer cells must halt proliferative pathways and reprogram their morphology and metabolism to metastasize from the primary tumor. Li et al. found that FUNDC1 played a role in suppressing the switch from proliferation to metastasis in cancer cells of different tissue origins. In mice, xenografts formed from FUNDC1-deficient cancer cells developed into smaller primary tumors but were more likely to metastasize. FUNDC1 promoted proliferation by suppressing fission and relocalization of mitochondria to the leading edge of migrating cancer cells, enhancing oxidative metabolism, and limiting mitochondrial ROS production. These effects required the stabilization of the mitochondrial protease LonP1 and components of the mitochondrial ATP synthase complex (also known as complex V) by FUNDC1. By regulating mitochondrial morphology, localization, and function, FUNDC1 confers the cellular and metabolic features that support cancer cell proliferation.

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