HDAC Inhibition Overcomes Acute Resistance to MEK Inhibition in <i>BRAF</i> -Mutant Colorectal Cancer by Downregulation of c-FLIPL

Abstract

Our findings indicate that c-MET/STAT3-dependent upregulation of c-FLIPL expression is an important escape mechanism following MEKi treatment in BRAFMT colorectal cancer. Thus, combinations of MEKi with inhibitors of c-MET or c-FLIP (e.g., HDAC inhibitors) could be potential novel treatment strategies for BRAFMT colorectal cancer.