Resveratrol modulation of signal transduction in apoptosis and cell survival: a mini-review |
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Authors: | Fulda Simone Debatin Klaus-Michael |
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Affiliation: | University Children's Hospital, Eythstr. 24, 89075 Ulm, Germany. simone.fulda@uniklinik-ulm.de |
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Abstract: | BACKGROUND: There is mounting evidence in the literature that resveratrol is a promising natural compound for prevention and treatment of a variety of human cancers. This overview summarizes recent studies of the major apoptosis and survival pathways regulated by resveratrol. BIOLOGICAL MECHANISMS: Apoptosis or programmed cell death is a key regulator of tissue homeostasis during normal development and also in adult organism under various conditions including adaptive responses to cellular stress. For example, tissue homeostasis is maintained by tight control of signaling events regulating cell death and survival. Thus, uncontrolled proliferation or failure to undergo cell death is involved in pathogenesis and progression of many human diseases, for example in tumorigenesis or in cardiovascular disorders. Moreover, current cancer therapies primarily act by triggering apoptosis programs in cancer cells. THERAPEUTIC APPLICATIONS: Natural products such as resveratrol have gained considerable attention as cancer chemopreventive or cardioprotective agents and also because of their antitumor properties. Among its wide range of biological activities, resveratrol has been reported to interfere with many intracellular signaling pathways, which regulate cell survival or apoptosis. DISCUSSION: Further insights into the signaling network and interaction points modulated by resveratrol may provide the basis for novel drug discovery programs to exploit resveratrol for the prevention and treatment of human diseases. |
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Keywords: | AIF, apoptosis inducing factor ERK, extracellular-signal-regulated protein kinase FADD, Fas-associated death domain IAPs, inhibitor of apoptosis proteins JNK, c-Jun NH2-terminal kinases MAPK, mitogen-activated protein kinases NF-kappaB, nuclear factor-kappaB PI3K, phosphoinositide 3-kinase Smac, second mitochondria-derived activator of caspase TNF, tumor necrosis factor TRAIL, TNF-related apoptosis-inducing ligand |
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