Metabolic vulnerability of KRAS-driven cancer cells

Abstract

Interfering with anaplerotic utilization of glutamine (Gln) was recently reported to sensitize KRAS-driven cancer cells to the cytotoxic effects of capecitabine and paclitaxel. This effect was due to bypass of a Gln-dependent G1 cell cycle checkpoint in these cells. This study highlights therapeutic opportunities created by metabolic reprogramming in cancer cells.