Fig. 3
From: Multiple roles of branched-chain amino acid metabolism in tumour progression
BCAA hypercatabolism promotes tumour development. BCAA metabolism maintains PRC2 activity by promoting the transcription of EZH2 and EED, thereby maintaining the dryness of acute leukaemia. High expression levels of BCAT1 lead to a decrease in α-KG levels, and promote the occurrence and development of leukaemia and lung cancer through epigenetic remodelling of the EGLN1-HIF1α axis, KDM4A/C-ATM axis and miR-200c-SOX2 axis. The BCAA-GCN2-EIF2α axis and the KRAS-SYK axis promote the development of pancreatic ductal adenocarcinoma by stabilizing BCAT2 and enhancing BCAA catabolism. On the one hand, ROS promotes the transcription of BCAT1 by activating HIF1; on the other hand, it up-regulates the expression of BCAT1 through the LDHA-DOT1L axis to increase the catabolism of BCAAs, resulting in an increase in the levels of the glutamate-derived antioxidants GSH and TxN, and maintaining the redox state of glioblastoma