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Hepatocellular carcinoma redirects to ketolysis for progression under nutrition deprivation stress
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Hepatocellular carcinoma redirects to ketolysis for progression under nutrition deprivation stress
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Journal Article
Hepatocellular carcinoma redirects to ketolysis for progression under nutrition deprivation stress
2016
Overview
Cancer cells are known for their capacity to rewire metabolic pathways to support survival and proliferation under various stress conditions. Ketone bodies, though produced in the liver, are not consumed in normal adult liver cells. We find here that ketone catabolism or ketolysis is re-activated in hepatocellular carcinoma （HCC） cells under nutrition deprivation conditions. Mechanistically, 3-oxoacid CoA-transferase 1 （OXCT1）, a rate-limiting ketolytic enzyme whose expression is suppressed in normal adult liver tissues, is re-induced by serum starvation-triggered mTORC2- AKT-SP1 signaling in HCC cells. Moreover, we observe that enhanced ketolysis in HCC is critical for repression of AMPK activation and protects HCC cells from excessive autophagy, thereby enhancing tumor growth. Importantly, analysis of clinical HCC samples reveals that increased OXCT1 expression predicts higher patient mortality. Taken together, we uncover here a novel metabolic adaptation by which nutrition-deprived HCC cells employ ketone bodies for energy supply and cancer progression.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Animals
/ Biomedical and Life Sciences
/ Carcinoma, Hepatocellular - metabolism
/ Carcinoma, Hepatocellular - mortality
/ Carcinoma, Hepatocellular - pathology
/ Cell Proliferation - drug effects
/ Coenzyme A-Transferases - antagonists & inhibitors
/ Coenzyme A-Transferases - genetics
/ Coenzyme A-Transferases - metabolism
/ Culture Media, Serum-Free - pharmacology
/ Humans
/ Hydroxybutyrates - metabolism
/ Ketones
/ Liver Neoplasms - metabolism
/ Mechanistic Target of Rapamycin Complex 2 - metabolism
/ Mice
/ Original
/ Proto-Oncogene Proteins c-akt - metabolism
/ Signal Transduction - drug effects
