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

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.

Bibliographic Details
Main Authors: David M. Walter, Amy C. Gladstein, Katherine R. Doerig, Ramakrishnan Natesan, Saravana G. Baskaran, A. Andrea Gudiel, Keren M. Adler, Jonuelle O. Acosta, Douglas C. Wallace, Irfan A. Asangani, David M. Feldser
Format: Article
Language:English
Published: Nature Portfolio 2023-03-01
Series:Communications Biology
Online Access:https://doi.org/10.1038/s42003-023-04618-3