What is it about?

Cancer cells without mitochondrial DNA (mtDNA) do not form tumors unless they can highjack host mitochondria. Authors show that the acquired mitochondrial electron transport is necessary to drive de novo pyrimidine synthesis to overcome cell-cycle arrest. Surprisingly, ATP generation is dispensable for tumorigenesis in this context. Authors show that the key enzyme dihydroorotate dehydrogenase (DHODH) provides a link between pyrimidine biosynthesis required for cancer cell proliferation and redox-cycling of coenzyme Q (CoQ) through functional OXPHOS.

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Why is it important?

Authors document sevral highlights: Tumorigenesis depends on functional OXPHOS OXPHOS-derived ATP is not required for tumor formation DHODH-driven pyrimidine biosynthesis requires CoQ redox cycling CoQ redox-cycling via OXPHOS drives tumorigenesis through pyrimidine biosynthesis

Perspectives

This research may initiate interest in the key molecular events linked to tumor initiation and the role of mitochondria in the process of tumorigenesis.

Jaroslav Truksa

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This page is a summary of: Reactivation of Dihydroorotate Dehydrogenase-Driven Pyrimidine Biosynthesis Restores Tumor Growth of Respiration-Deficient Cancer Cells, Cell Metabolism, February 2019, Elsevier,
DOI: 10.1016/j.cmet.2018.10.014.
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