ACE2 negatively regulates the Warburg effect and suppresses hepatocellular carcinoma progression via reducing ROS-HIF1α activity
Fangyuan Dong, Hui Li, Limin Liu, Linli Yao, Jiaofeng Wang, Danni Xiang, Jianxia Ma, Gansheng Zhang, Shan Zhang, Jun Li, Shu‐Heng Jiang, Xiaona Hu, Jie Chen, Zhijun Bao
Abstract
additive tumor growth and aerobic glycolysis induced by ACE2 knockdown. Moreover, growth advantages afforded by ACE2 knockdown are largely glycolysis-dependent. In clinical settings, a close link between ACE2 expression and HIF1α or the phosphorated level of SHP2 is found. Overexpression of ACE2 significantly retards tumor growth in patient-derived xenograft model. Collectively, our findings suggest that ACE2 is a negative glycolytic regulator, and targeting the ACE2/Ang-(1-7)/Mas receptor/ROS/HIF1α axis may be a promising therapeutic strategy for HCC treatment.
Topics & Concepts
GlycolysisAnaerobic glycolysisGene knockdownWarburg effectCancer researchBiologyCell biologyChemistryBiochemistryApoptosisMetabolismCancer, Hypoxia, and MetabolismPhysiological and biochemical adaptationsAdvanced Proteomics Techniques and Applications