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The novel resveratrol analogue HS-1793 induces apoptosis via the mitochondrial pathway in murine breast cancer cells
Author(s) -
Hyoun-Ji Kim,
Kwangmo Yang,
YOO-SOO PARK,
Yoo-Jin Choi,
JiHyeon Yun,
CheolHun Son,
Hongsuk Suh,
MinHo Jeong,
WolSoon Jo
Publication year - 2012
Publication title -
international journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.405
H-Index - 122
ISSN - 1019-6439
DOI - 10.3892/ijo.2012.1615
Subject(s) - apoptosis , resveratrol , cytotoxicity , cytochrome c , biology , mitochondrion , cancer cell , programmed cell death , cancer research , cancer , oncogene , cytotoxic t cell , caspase , cell cycle , poly adp ribose polymerase , pharmacology , microbiology and biotechnology , biochemistry , in vitro , enzyme , genetics , polymerase
Resveratrol (3,4',5 tri-hydroxystilbene), a natural plant polyphenol, hasgained interest as a non-toxic chemopreventive agent capable of inducing tumorcell death in a variety of cancer types. Several studies were undertaken to obtainsynthetic analogues of resveratrol with potent anticancer activity. The aim ofthe present study was to investigate the effect of HS-1793 as a new resveratrolanalog on apoptosis via the mitochondrial pathway in murine breast cancer cells.A pharmacological dose (1.3-20 µM) of HS-1793 exerted a cytotoxic effect on murinebreast cancer cells resulting in apoptosis. HS-1793-mediated cytotoxicity in FM3Acells by several apoptotic events including mitochondrial cytochrome c release,activation of caspase-3 and PARP occurred. In addition, HS-1793 induced collapseof ∆Ψm and enhanced AIF and Endo G release from mitochondria while undergoingapoptosis. These results demonstrate that the cytotoxicity by HS-1793 in FM3Acells can mainly be attributed to apoptosis via a mitochondrial pathway by caspaseactivation or contributions of AIF and Endo G.

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