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Piceatannol induces apoptosis through death receptor and mitochondrion‐dependent pathways in human prostate cancer cells
Author(s) -
Park Heesook,
Kim Eun Ji,
Park So Young,
Kwon Dae Young,
Park Jung Han Yoon
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.700.21
Subject(s) - piceatannol , du145 , lncap , apoptosis , chemistry , programmed cell death , cancer research , poly adp ribose polymerase , cytochrome c , caspase 3 , microbiology and biotechnology , cancer cell , biology , biochemistry , resveratrol , medicine , cancer , enzyme , polymerase
Piceatannol (3,3′,4,5′‐tetrahydroxy‐trans‐stilbene) is a polyphenol found in grapes, red wine, and Rheum undulatum. Previous studies by others showed that piceatannol inhibits proliferation of various cancer cells. In this study we examined the effects of piceatannol on the growth of androgen‐sensitive LNCaP and androgen‐insensitive DU145 prostate cancer cells. Piceatannol decreased the viable numbers of DU145 and LNCaP cells and increased apoptotic cell numbers in a dose‐dependent manner. Western blot analysis revealed that piceatannol increased the protein levels of cleaved caspase‐8, ‐9, ‐7 and ‐3 and cleaved poly (ADP‐ribose) polymerase (PARP). Piceatannol increased mitochondrial membrane permeability and release of cytochrome c from mitochondria to cytosol. Piceatannol increased the levels of truncated‐Bid, Bax, Bik, Bok and Fas but decreased the levels of Mcl‐1 and Bcl‐xL. Caspase‐8 and caspase‐9 inhibitors mitigated piceatannol‐induced apoptosis. The caspase‐8 inhibitor suppressed piceatannol‐induced cleavage of Bid, caspase‐9, caspase‐3 and PARP. These results suggest that piceatannol induces apoptosis through the death receptor and mitochondrial dependent pathways.