Mitochondrial p32 protein is a critical regulator of tumor metabolism via maintenance of oxidative phosphorylation
Authors: Jeffrey W Smith
Priya P Karmali
Erkki Ruoslahti
Immo E Scheffler
Adam D Richardson
Valentina Fogal
Journal: Molecular and Cellular Biology (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p32; gC1qR; C1QBP; HABP1; cancer cells
Affiliations: Cancer Research Center, Burnham Institute for Medical Research, 10901 N Torrey Pines Rd, La Jolla, California 92037, USA., Cancer Research Center, Burnham Institute for Medical Research, 10901 N. Torrey Pines Rd., La Jolla, California 92037, Division of Biology, Molecular Biology Section, University of California, San Diego, La Jolla, California 92093-0322, Vascular Mapping Center, Burnham Institute for Medical Research at UCSB, 1105 Life Sciences Technology Bldg., University of California, Santa Barbara, Santa Barbara, California 93106-9610

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. 

Retracted: No

PubPeer comments:
 2017 correction. http: mcb.asm.org content 37 14 e00137-17.short , 
 The correction reads:  *Fig. 9A, center panel: The control wells below the graph were an unintentional duplication of the u201cmicellesu201d wells from panel B. The correct wells are shown below. We regret these errors. However, since the microtiter wells were shown for illustrative purposes and the corresponding quantification of lactate production from multiple experiments was also shown, this duplication ultimately does not affect the interpretation of the experiments or the conclusions of the study.* Here are the duplications in the original Figure 9, marked by red boxes. Reported to the journal in September 2016. ![file] I thank the authors for correcting this error. This paper was part of a structured search for image duplications in Molecular and Cellular Biology paper, which was published here: https: mcb.asm.org content 38 20 e00309-18.long , 
 #2  the microtiter wells were shown for illustrative purposes It would be appreciated if authors generally limited their figures to presenting data relevant to the conclusions as opposed to including illustrations solely for the reader s enjoyment. It is easy to see the illustration above and believe that the authors intended to show images of actual experiments. ,