Ontology type: schema:ScholarlyArticle Open Access: True
2016-12
AUTHORSYujun Hao, Yardena Samuels, Qingling Li, Dawid Krokowski, Bo-Jhih Guan, Chao Wang, Zhicheng Jin, Bohan Dong, Bo Cao, Xiujing Feng, Min Xiang, Claire Xu, Stephen Fink, Neal J. Meropol, Yan Xu, Ronald A. Conlon, Sanford Markowitz, Kenneth W. Kinzler, Victor E. Velculescu, Henri Brunengraber, Joseph E. Willis, Thomas LaFramboise, Maria Hatzoglou, Guo-Fang Zhang, Bert Vogelstein, Zhenghe Wang
ABSTRACTCancer cells often require glutamine for growth, thereby distinguishing them from most normal cells. Here we show that PIK3CA mutations reprogram glutamine metabolism by upregulating glutamate pyruvate transaminase 2 (GPT2) in colorectal cancer (CRC) cells, making them more dependent on glutamine. Compared with isogenic wild-type (WT) cells, PIK3CA mutant CRCs convert substantially more glutamine to α-ketoglutarate to replenish the tricarboxylic acid cycle and generate ATP. Mutant p110α upregulates GPT2 gene expression through an AKT-independent, PDK1-RSK2-ATF4 signalling axis. Moreover, aminooxyacetate, which inhibits the enzymatic activity of aminotransferases including GPT2, suppresses xenograft tumour growth of CRCs with PIK3CA mutations, but not with WT PIK3CA. Together, these data establish oncogenic PIK3CA mutations as a cause of glutamine dependency in CRCs and suggest that targeting glutamine metabolism may be an effective approach to treat CRC patients harbouring PIK3CA mutations. More... »
PAGES11971
http://scigraph.springernature.com/pub.10.1038/ncomms11971
DOIhttp://dx.doi.org/10.1038/ncomms11971
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PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/27321283
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