Oncogenic signaling upstream of mTORC1 drives lipogenesis and proliferation through SREBP

Background The mechanistic target of rapamycin (mTOR) is a central regulator of cell growth and proliferation, and its aberrant activation is frequent in cancer [1]. We have previously shown that sterol regulatory element binding protein (SREBP) is a major transcriptional effector of mTOR complex 1 (mTORC1) signaling [2]. SREBP is a transcription factor that stimulates the expression of genes involved in the de novo synthesis of lipids [3]. Since mTORC1 is commonly activated in cancer through upstream oncogenic signaling pathways and enhanced lipogenesis is a metabolic hallmark of tumor cells, we hypothesize that the mTORC1-SREBP pathway is important for tumor metabolism and growth.