Dietary energy balance modulation of epithelial carcinogenesis: a role for IGF-1 receptor signaling and crosstalk

摘要: Obesity affects more than one third of the U.S. population and is associated with increased risk and/or disease severity for several chronic diseases, including cancer. In contrast, calorie restriction (CR) consistently inhibits cancer across species types. Differential effects on globally active circulatory proteins, particularly insulin-like growth factor-1 (IGF-1), provide a plausible mechanistic explanation energy balance–cancer link. Diet-induced changes in circulating IGF-1 modulate IGF-1R/EGFR activation downstream signaling to Akt mTOR. These dietary balance ultimately levels activity cell cycle regulatory regulating proliferation, modulating susceptibility tumor development. Selective targeting mTORC1 potently tumorigenesis model systems producing CR mimetic effects. Targeting this other pathways modulated by may lead development strategies chemoprevention reversing obesity progression.