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.
Keywords: MAX; MLXIP; MONDOA MLX; MYC; MYCN; cancer; glucose; lipid; metabolism.