Cancer Communications
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BMC

Inhibitory effect of cucurbitacin E on the proliferation of ovarian cancer cells and its mechanism
Xiao-Lei Shan, Xue-Ying Zhou, Jiao Yang, Yan-Li Wang, Yi-Hui Deng , Mei-Xia Zhang
Department of Clinical Pharmacology, China Medical University, Shenyang, 110001, Liaoning, P. R. China. meixia_zhang@yahoo.com
[Abstract] Background and Objective: There are various biological activities of cucurbitacin E (CuE), including antitumor effect, anti-chemical carcino-genesis, liver-protection, and enhancement of the immunity, and so on. This study was to investigate the effect of CuE on proliferation inhibition and apoptosis induction of ovarian cancer ES-2 cells, and to explore the mechanism. Methods: ES-2 cells were treated with different concentrations of CuE for 24, 48, and 72 h, respectively , and cell proliferation was detected by MTT assay. The morphological changes and apoptosis were observed under inverted microscopy and fluorescent microscopy. Cell cycle distribution was analyzed by flow cytometry. The expression of pSTAT3 was determined by Western blot. Results: The number of ES-2 cells significantly decreased as the concentration of CuE increased or the time prolonged. Flow cytometry analysis showed that the ratio of ES-2 cells treated with 1 &mgr;mol/L CuE for 24 h increased both in S phase [from (10.55±0.91)% to (16.31±4.61)%] and in G2/M phase [from (18.53±1.43)% to (58.34±5.77)%], while decreased in G1 phase [from (73.13±4.70)% to (23.12±5.45)%] (P<0.05). The marked morphological changes of cell apoptosis were clearly observed in ES-2 cells treated with CuE. CuE inhibited the STAT3 phosphorylation in ES-2 cells in a dose-dependent manner. Conclusion: CuE can inhibit ES-2 cell proliferation and induce apoptosis and cell cycle arrest, which may be related to the decreased expression of the intracellular STAT3 phosphorylation.
Chinese Journal of Cancer 2010, Volume: 29, Issue 1, Page: 20-
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