Rugosin E, an ellagitannin, inhibits MDA-MB-231 human breast cancer cell proliferation and induces apoptosis by inhibiting nuclear factor-κB signaling pathway.

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Title:	Rugosin E, an ellagitannin, inhibits MDA-MB-231 human breast cancer cell proliferation and induces apoptosis by inhibiting nuclear factor-κB signaling pathway.
Authors:	Po-Lin Kuo Ya-Ling Hsu Ta-Chen Lin Wen-Sheng Tzeng Yin-Yi Chen Chun-Ching Lin
Contributors:	生物科技系
Keywords:	Rugosin E Breast cancer Apoptosis Cell cycle NF-κB
Date:	2007-04
Issue Date:	2010-01-12 09:13:11 (UTC+8)
Abstract:	In this study, we first report the chemopreventive effect of rugosin E in human breast cancer cell line, MDA-MB-231. Treatment with rugosin E decreased the cell proliferation of MDA-MB-231 cells in a dose-dependent manner. Rugosin E treatment arrested MDA-MB-231 cells at G0/G1 phase. This effect was strongly associated with concomitant decrease in the level of cyclin D1, cyclin D2, cyclin E, cdk2, cdk4, and cdk6, and increase of p21/WAF1. In addition, rugosin E also induced apoptotic cell death. Rugosin E increased in the expression of Bax, Bak, and Bcl-Xs, but decreased the levels of Bcl-2 and Bcl-XL, and subsequently triggered mitochondria apoptotic pathway (release of cytochrome c, activation of caspase-9, and caspase-3). In addition, pre-treatment of cells with caspase-9 inhibitor blocked rugosin E-induced cell proliferation and apoptosis, indicating caspase-9 activation was involved in rugosin E-mediated MDA-MB-231 cells apoptosis. Rugosin E inhibited the constitutively activated and inducible NF-κB in both its DNA-binding activity and transcriptional activity. Furthermore, rugosin E also inhibited the TNF-α-activated NF-κB-dependent reporter gene expression of cyclin D1, c-Myc, XIAP, Bcl-2, and Bcl-XL were all downregulated by rugosin E. Our results indicated that rugosin E inhibits the activation of NF-κB, and this may provide a molecular basis for drug development in the prevention and treatment of cancer by rugosin E.
Relation:	Cancer letters 248(2)： p.280-291
Appears in Collections:	[Dept. of Biotechnology (including master's program)] Periodical Articles

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