c-Src Promotes Tumorigenesis and Tumor Progression by Activating PFKFB3
Huanhuan Ma, Jia Zhang, Lin Zhou, Shixiong Wen, Hsiang-Yu Tang, Bin Jiang, Fengqiong Zhang, Muhammad Suleman, Dachao Sun, Ai Chen, Wentao Zhao, Furong Lin, Ming-Tong Tsau, Lu-Min Shih, Changchuan Xie, Xiaotong Li, Donghai Lin, Li‐Man Hung, Mei‐Ling Cheng, Qinxi Li
Abstract
mice. In summary, we identify a specific mechanism by which c-Src mediates glucose metabolism to meet cancer cells' requirements for maximal biosynthesis and proliferation. The PFKFB3-Tyr194 phosphorylation level highly correlates with c-Src activity in clinical tumor samples, indicating its potential as an evaluation for tumor prognosis.
Topics & Concepts
Pentose phosphate pathwayGlycolysisCarcinogenesisCell biologyCancer researchProto-oncogene tyrosine-protein kinase SrcPhosphorylationOxidative phosphorylationTumor progressionBiologyCancer cellCancerChemistryBiochemistryMetabolismGeneticsCancer, Hypoxia, and MetabolismMetabolism, Diabetes, and CancerMitochondrial Function and Pathology