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Your search keyword '"Yin, Yi"' showing total 2 results
Start Over Author "Yin, Yi" Topic apoptosis Journal cancer letters
2 results on '"Yin, Yi"'

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

Author

Kuo PL, Hsu YL, Lin TC, Tzeng WS, Chen YY, and Lin CC

Subjects
Blotting, Western, Breast Neoplasms metabolism, Cell Cycle drug effects, Cell Cycle Proteins drug effects, Cell Line, Tumor, Cell Proliferation drug effects, Dose-Response Relationship, Drug, Electrophoretic Mobility Shift Assay, Female, Humans, NF-kappa B metabolism, Reverse Transcriptase Polymerase Chain Reaction, Apoptosis drug effects, Breast Neoplasms prevention & control, Hydrolyzable Tannins pharmacology, NF-kappa B drug effects, Signal Transduction drug effects
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-X(L), 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-kappaB in both its DNA-binding activity and transcriptional activity. Furthermore, rugosin E also inhibited the TNF-alpha-activated NF-kappaB-dependent reporter gene expression of cyclin D1, c-Myc, XIAP, Bcl-2, and Bcl-X(L) were all downregulated by rugosin E. Our results indicated that rugosin E inhibits the activation of NF-kappaB, and this may provide a molecular basis for drug development in the prevention and treatment of cancer by rugosin E.

Published
2007
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2. Rugosin E, an ellagitannin, inhibits MDA-MB-231 human breast cancer cell proliferation and induces apoptosis by inhibiting nuclear factor-kappaB signaling pathway

Author

Yin-Yi Chen, Chun-Ching Lin, Ta-Chen Lin, Po-Lin Kuo, Wen-Sheng Tzeng, and Ya-Ling Hsu

Subjects
Cancer Research, Cyclin E, Blotting, Western, Apoptosis, Breast Neoplasms, Cell Cycle Proteins, Electrophoretic Mobility Shift Assay, Biology, Cyclin D1, Cyclin D2, Cell Line, Tumor, Humans, Cell Proliferation, Dose-Response Relationship, Drug, Cell growth, Reverse Transcriptase Polymerase Chain Reaction, Cell Cycle, NF-kappa B, Cell cycle, Hydrolyzable Tannins, XIAP, Cell biology, Oncology, Cancer research, biology.protein, Female, Cyclin-dependent kinase 6, Signal Transduction
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-X(L), 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-kappaB in both its DNA-binding activity and transcriptional activity. Furthermore, rugosin E also inhibited the TNF-alpha-activated NF-kappaB-dependent reporter gene expression of cyclin D1, c-Myc, XIAP, Bcl-2, and Bcl-X(L) were all downregulated by rugosin E. Our results indicated that rugosin E inhibits the activation of NF-kappaB, and this may provide a molecular basis for drug development in the prevention and treatment of cancer by rugosin E.

Published
2006

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