Our understanding of how the RAS protein family, and in particular mutant KRAS promote metabolic dysregulation in cancer cells has advanced significantly over the last decade. In this Review, we discuss the metabolic reprogramming mediated by oncogenic RAS in cancer, and elucidating the underlying mechanisms could translate to novel therapeutic opportunities to target metabolic vulnerabilities in RAS-driven cancers.
Keywords: KRAS; autophagy; cancer therapeutics; chemoresistance; ferroptosis; glutaminolysis; glycolysis; macropinocytosis; metabolism.