A novel role for the extended MYC network in cancer cell survival.
Cancer cells exhibit altered metabolic requirements compared to their normal counterparts. This metabolic reprogramming is mediated by activation of oncogenes such as MYC. Here, we summarize our recent findings demonstrating a metabolic dependency of deregulated MYC on MLXIP-MLX, critical components of the nutrient-sensing arm of the extended MYC transcriptional network.
Division of Basic Sciences, Fred Hutchinson Cancer Research Center ; Seattle, WA, USA.
Patrick A
PA
Carroll
Division of Basic Sciences, Fred Hutchinson Cancer Research Center ; Seattle, WA, USA.
Daniel
D
Diolaiti
MAX; MLXIP; MONDOA MLX; MYC; MYCN; cancer; glucose; lipid; metabolism