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Journal of Oncology
Volume 2013 (2013), Article ID 872957, 9 pages
http://dx.doi.org/10.1155/2013/872957
Research Article

Enhancement of Cisplatin-Mediated Apoptosis in Ovarian Cancer Cells through Potentiating G2/M Arrest and p21 Upregulation by Combinatorial Epigallocatechin Gallate and Sulforaphane

1Department of Biology, University of Alabama at Birmingham, CH175, 1300 University Boulevard, Birmingham, AL 35294-1170, USA
2Department of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
3Center for Aging, University of Alabama at Birmingham, Birmingham, AL 35294, USA
4Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA
5Nutrition Obesity Research Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA
6Comprehensive Diabetes Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA

Received 19 December 2012; Accepted 10 January 2013

Academic Editor: Jorg Kleeff

Copyright © 2013 Huaping Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Advanced-stage ovarian cancer is characterized by high mortality due to development of resistance to conventional chemotherapy. Novel compounds that can enhance the efficacy of conventional chemotherapy in ovarian cancer may overcome this drug resistance. Consumption of green tea (epigallocatechin gallate, EGCG) and cruciferous vegetables (sulforaphane, SFN) is inversely associated with occurrence of ovarian cancer and has anticancer effects through targeting multiple molecules in cancer cells. However, the effects of EGCG and SFN combinational treatment on ovarian cancer cells and on efficacy of cisplatin to these cells are unknown. In this study, EGCG or SFN was used to treat both cisplatin-sensitive (A2780) and cisplatin-resistant (A2780/CP20) ovarian cancer cells alone or in combination with cisplatin. We found that EGCG and SFN combinational treatment can reduce cell viability of both ovarian cancer cell lines time- and dose-dependently. Furthermore, EGCG and SFN combinational treatment can enhance cisplatin-induced apoptosis and G2/M phase arrest, thereby enhancing the efficacy of cisplatin on both cisplatin-sensitive and cisplatin-resistant ovarian cancer cells. EGCG and SFN combinational treatment upregulated p21 expression induced by cisplatin in cisplatin-sensitive ovarian cancer cells, while p27 expression was not regulated by these treatments. Collectively, these studies provide novel approaches to overcoming cisplatin chemotherapy resistance in ovarian cancer.