Targeting the BCKDK/BCLAF1/MYC/HK2 axis to alter aerobic glycolysis and overcome Trametinib resistance in lung cancer

BCKDK is a branched-chain amino acid metabolizing enzyme whose expression is up-regulated in tumors. BCKDK is closely associated with the development, progression, and metastasis of a wide range of tumors; however, the mechanisms behind this association remain poorly understood. To explore the pro-tumorigenic molecular mechanism of BCKDK, we performed RNA sequencing analysis of BCKDK-deficient H1299 cells. Overall design: BCKDK stable knockout (KO) cell lines were generated by Clustered regularly interspaced short palindromic repeat (CRISPR) genome editing.Two monoclonal cell lines were obtained by limited dilution.Cells with lentiviral transduction of the lentiCRISPR v2 plasmid served as controls.