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Mol Cell Biol. 2010 Mar;30(6):1303-18. doi: 10.1128/MCB.01101-09. Epub 2010 Jan 25.

Mitochondrial p32 protein is a critical regulator of tumor metabolism via maintenance of oxidative phosphorylation.

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  • 1Cancer Research Center, Burnham Institute for Medical Research, 10901 N Torrey Pines Rd, La Jolla, California 92037, USA.

Abstract

p32/gC1qR/C1QBP/HABP1 is a mitochondrial/cell surface protein overexpressed in certain cancer cells. Here we show that knocking down p32 expression in human cancer cells strongly shifts their metabolism from oxidative phosphorylation (OXPHOS) to glycolysis. The p32 knockdown cells exhibited reduced synthesis of the mitochondrial-DNA-encoded OXPHOS polypeptides and were less tumorigenic in vivo. Expression of exogenous p32 in the knockdown cells restored the wild-type cellular phenotype and tumorigenicity. Increased glucose consumption and lactate production, known as the Warburg effect, are almost universal hallmarks of solid tumors and are thought to favor tumor growth. However, here we show that a protein regularly overexpressed in some cancers is capable of promoting OXPHOS. Our results indicate that high levels of glycolysis, in the absence of adequate OXPHOS, may not be as beneficial for tumor growth as generally thought and suggest that tumor cells use p32 to regulate the balance between OXPHOS and glycolysis.

Comment in

PMID:
20100866
[PubMed - indexed for MEDLINE]
PMCID:
PMC2832503
Free PMC Article

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