Loss of Abhd5 Promotes Colorectal Tumor Development and Progression by Inducing Aerobic Glycolysis and Epithelial-Mesenchymal Transition

• DOI: 10.1016/j.celrep.2014.11.016
• Publication Date: 2014-12-04T18:28:00Z
• Authors: Juanjuan Ou; Hongming Miao; Yinyan Ma; Feng Guo; Jia Deng; Xing Wei; Jie Zhou; Ganfeng Xie; Hang Shi; Bingzhong Xue; Houjie Liang; Liqing Yu
• Keywords: Anaerobic glycolysis; Warburg Effect; Lipid droplet

How cancer cells shift metabolism to aerobic glycolysis is largely unknown. Here, we show that deficiency of α/β-hydrolase domain-containing 5 (Abhd5), an intracellular lipolytic activator also known as comparative gene identification 58 (CGI-58), promotes this metabolic and enhances malignancies colorectal carcinomas (CRCs). Silencing Abhd5 in normal fibroblasts induces malignant transformation. Intestine-specific knockout Apc(Min/+) mice robustly increases tumorigenesis transformation adenomatous polyps. In colon cells, epithelial-mesenchymal transition by suppressing the AMPKα-p53 pathway, which attributable increased glycolysis. human CRCs, expression falls substantially correlates negatively with features. Our findings link CRC pathogenesis suggest develop Abhd5-mediated lipolysis.