The novel resveratrol analogue HS-1793 induces apoptosis via the mitochondrial pathway in murine breast cancer cells.

Abstract

Resveratrol (3,4',5 tri-hydroxystilbene), a natural plant polyphenol, has gained interest as a non-toxic chemopreventive agent capable of inducing tumor cell death in a variety of cancer types. Several studies were undertaken to obtain synthetic analogues of resveratrol with potent anticancer activity. The aim of the present study was to investigate the effect of HS-1793 as a new resveratrol analog 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 murine breast cancer cells resulting in apoptosis. HS-1793-mediated cytotoxicity in FM3A cells by several apoptotic events including mitochondrial cytochrome c release, activation of caspase-3 and PARP occurred. In addition, HS-1793 induced collapse of ∆Ψm and enhanced AIF and Endo G release from mitochondria while undergoing apoptosis. These results demonstrate that the cytotoxicity by HS-1793 in FM3A cells can mainly be attributed to apoptosis via a mitochondrial pathway by caspase activation or contributions of AIF and Endo G.

• Authors: Hyoun-Ji Kim, Kwang-Mo Yang, Yoo-Soo Park, Yoo-Jin Choi, Ji-Hyeon Yun, Cheol-Hun Son, Hong-Suk Suh, Min-Ho Jeong, Wol-Soon Jo
• Journal: International journal of oncology (Int J Oncol) Vol. 41 Issue 5 Pg. 1628-34 (Nov 2012) ISSN: 1791-2423 [Electronic] Greece
• PMID: 22940714 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• 4-(6-hydroxy-2-naphthyl)-1,3-benzenediol
• Antineoplastic Agents
• Naphthols
• Resorcinols
• Cytochromes c
• Poly(ADP-ribose) Polymerases
• Caspase 3

Topics

• Animals
• Antineoplastic Agents (pharmacology)
• Apoptosis (drug effects)
• Breast Neoplasms (metabolism)
• Caspase 3 (metabolism)
• Cell Line, Tumor
• Cell Survival (drug effects)
• Cytochromes c (metabolism)
• Female
• G1 Phase (drug effects)
• Membrane Potential, Mitochondrial (drug effects)
• Mice
• Mitochondria (drug effects, metabolism)
• Naphthols (pharmacology)
• Poly(ADP-ribose) Polymerases (metabolism)
• Resorcinols (pharmacology)
• Signal Transduction (drug effects)