Setd2 inactivation sensitizes lung adenocarcinoma to inhibitors of oxidative respiration and mTORC1 signaling

Abstract

SETD2 inactivation leads to heightened mTORC1 signaling, oxidative metabolism and protein synthesis in KRAS-driven mouse models of lung adenocarcinoma, contributing to the understanding of how SETD2 deficiency drives early and widespread tumor growth.