Pan-HDAC Inhibition Reverses the Warburg Effect and Leads to Metabolic Vulnerabilities

We report the HDAC inhibiton of glioblastoma cells causes histone H3K27 acetylation and leads to upreguated OXPHOS master regulator PGC1a which then leads to an increase in mitochondrial fusion, mitochondrial biogenesis and higher mitochondrial oxygen consumption rate coupled with increased fatty acid oxidation (FAO). Overall design: Examination of histone H3K27ac modifications and RNA polymerase accumulating in 3 cell types under control or drug treated condition