Genome-wide analysis of gene expression in U87MG with different succinyaltion levels

NADP+-IDH mutations-produced R-2-hydroxylglutarate induces mitochondrial hypersuccinylation that induces cancerous metabolism and apoptosis resistance. Relief of hypersuccinylation inhibits tumorigenic growth of IDH mutant-harboring cells. Determination on transcriptional level of cells which were hypersuccinyalted helped us understand the mechanism, and we tested the hypothesis that IDH1R132H mutant affects cells through inducing hypersuccinylation by comparing R132H- overexpressing cells with cells in which the desuccinyaltase, SIRT5, were knocked down or the SIRT5 were overexpressed together with R132H. Total RNA obtained from cells overexpressing R132H compared to SIRT5KD cells, or R132H&SIRT5 overexpressing cells