Figure 1.

Potential molecular mechanisms involved in pterostilbene-induced cancer cell death. The multiple molecular interactions and signaling mechanisms are based on or deduced from data obtained in metastatic melanoma cells under in vivo conditions. Pterostilbene (PT) is encircled, and its interactions (inhibitions or activations are indicated by a T line or an arrow, respectively). Abbreviations: iNOS, inducible nitric oxide synthase; nitric oxide, NO; guanylate cyclase, GNC; CAMP responsive element binding protein, CREB; signal transducer and activator of transcription 3, STAT3; B-cell lymphoma 2, Bcl2; B-cell lymphoma-extra large, BclxL; tumor protein p53, p53; Bcl2-assciated X protein, Bax; adrenocorticotropic hormone, ACTH; glucocorticoid, GC; glucocorticoid receptor, GR; nuclear factor erythroid 2-related factor 2, Nrf2; Kelch-like ECH-associated protein 1, Keap1; protein kinase C PKC; mitogen-activated protein kinase, MAPK; phosphoinositide 3 kinase/protein kinase B/mechanistic target of rapamycin, PI3/AKT/mTOR; endothelial nitric oxide synthase, eNOS; reactive oxygen species, ROS; neutral sphingomyelinase, NSMase; mitochondrial permeability transition, MPT; nuclear factor kappa-light-chain-enhancer of activated B cells, NF-kB; nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, IkB; cyclooxygenase 2, COX2; TNF receptor-associated factor 2, TRAF2; inhibitors of apoptosis proteins, IAP.