AKT1 and MYC induce distinctive metabolic fingerprints in human prostate cancer

Cancer Research
Carmen PrioloMassimo Loda

Abstract

Cancer cells may overcome growth factor dependence by deregulating oncogenic and/or tumor-suppressor pathways that affect their metabolism, or by activating metabolic pathways de novo with targeted mutations in critical metabolic enzymes. It is unknown whether human prostate tumors develop a similar metabolic response to different oncogenic drivers or a particular oncogenic event results in its own metabolic reprogramming. Akt and Myc are arguably the most prevalent driving oncogenes in prostate cancer. Mass spectrometry-based metabolite profiling was performed on immortalized human prostate epithelial cells transformed by AKT1 or MYC, transgenic mice driven by the same oncogenes under the control of a prostate-specific promoter, and human prostate specimens characterized for the expression and activation of these oncoproteins. Integrative analysis of these metabolomic datasets revealed that AKT1 activation was associated with accumulation of aerobic glycolysis metabolites, whereas MYC overexpression was associated with dysregulated lipid metabolism. Selected metabolites that differentially accumulated in the MYC-high versus AKT1-high tumors, or in normal versus tumor prostate tissue by untargeted metabolomics, were validated u...Continue Reading

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Related Concepts

AKT1 protein, human
Founder Mice, Transgenic
Neoplasm Proteins
Malignant Neoplasm of Prostate
Tumor Markers
Gene Expression Regulation, Neoplastic
N-Myc Protein
Protein kinase B gamma
Metabolic Networks and Pathways
Gleason Grading System

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