期刊
CELL REPORTS
卷 9, 期 5, 页码 1798-1811出版社
CELL PRESS
DOI: 10.1016/j.celrep.2014.11.016
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资金
- National Institute of Diabetes and Digestive and Kidney Diseases [R01DK085176, R01DK084172]
- National Heart, Lung and Blood Institute [R01HL107500]
- National Natural Science Foundation of China [81370063, 81172115]
- China National Natural Science Foundation, Oversea, Hong Kong & Macao Scholars Collaborated Research Fund [510025]
How cancer cells shift metabolism to aerobic glycolysis is largely unknown. Here, we show that deficiency of alpha/beta-hydrolase domain-containing 5 (Abhd5), an intracellular lipolytic activator that is also known as comparative gene identification 58 (CGI- 58), promotes this metabolic shift and enhances malignancies of colorectal carcinomas (CRCs). Silencing of Abhd5 in normal fibroblasts induces malignant transformation. Intestine- specific knockout of Abhd5 in Apc(Min/+) mice robustly increases tumorigenesis and malignant transformation of adenomatous polyps. In colon cancer cells, Abhd5 deficiency induces epithelial-mesenchymal transition by suppressing the AMPK alpha-p53 pathway, which is attributable to increased aerobic glycolysis. In human CRCs, Abhd5 expression falls substantially and correlates negatively with malignant features. Our findings link Abhd5 to CRC pathogenesis and suggest that cancer cells develop aerobic glycolysis by suppressing Abhd5-mediated intracellular lipolysis.
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