Caloric restriction and cancer: molecular mechanisms and clinical implications  Ophélie Meynet, Jean-Ehrland Ricci  Trends in Molecular Medicine  Volume 20, Issue 8, Pages 419-427 (August 2014) DOI: 10.1016/j.molmed.2014.05.001 Copyright © 2014 Elsevier Ltd Terms and Conditions

Figure 1 Molecular pathways induced by caloric restriction to inhibit cancer. Caloric restriction (CR) can inhibit IGF-1/AKT and mTORC1 and activate AMPK, SIRT1, and SIRT3, suggesting that CR uses longevity pathways to limit cancer. The regulation of SIRT4 and SIRT6 by CR remains uncertain. Although the anticancer role for SIRT1, SIRT3, SIRT4, and SIRT6 is controversial, the crosstalk between AMPK and SIRTs is clearly established: AMPK can induce activation of SIRT1 via NAMPT and SIRT1 can activate AMPK via LKB1 regulation. The actions of three pharmacological mimics of CR (resveratrol, metformin, and rapamycin) are also indicated. Abbreviations: IGF-1, insulin-like growth factor 1; PI3K, phosphoinositide 3-kinase; mTORC1, mammalian target of rapamycin complex 1; NAMPT, nicotinamide phosphoribosyltransferase; SIRT, sirtuin; LKB1, liver kinase B1. Trends in Molecular Medicine 2014 20, 419-427DOI: (10.1016/j.molmed.2014.05.001) Copyright © 2014 Elsevier Ltd Terms and Conditions