Inhibitory effect of cucurbitacin E on the proliferation of ovarian cancer cells and its mechanism.
- Author:
Xiao-Lei SHAN
1
;
Xue-Ying ZHOU
;
Jiao YANG
;
Yan-Li WANG
;
Yi-Hui DENG
;
Mei-Xia ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents, Phytogenic; administration & dosage; pharmacology; Apoptosis; drug effects; Cell Cycle; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Dose-Response Relationship, Drug; Female; Humans; Ovarian Neoplasms; metabolism; pathology; Phosphorylation; STAT3 Transcription Factor; metabolism; Time Factors; Triterpenes; administration & dosage; pharmacology
- From:Chinese Journal of Cancer 2010;29(1):20-24
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND AND OBJECTIVEThere 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.
METHODSES-2 cells were treated with different concentrations of CuE for 24, 48, and 72 h, respectively. Cell proliferation was tested by MTT assay. The morphologic changes and apoptosis were observed under inverted microscope and fluorescent microscope. Cell cycle distribution was evaluated with flow cytometry. The expression of p-STAT3 was determined by Western blot.
RESULTSThe number of ES-2 significantly decreased as the concentration of CuE increased or the time prolonged. Flow cytometry analysis showed that the ratio of ES-2 cells treated 1 micromol/L CuE for 24 h increased both in S phase [from (10.55+/-0.91)% to ( 16.31 +/- 4.61) % ] and in G(2)/M phase [from (18.53+/-1.43)% to (58.34 +/- 5.77)%], while decreased in G(1) 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 cell in a dose- dependent manner.
CONCLUSIONCuE can inhibit ES-2 proliferation and induce apoptosis and cell cycle arrest, which may be related to the decreased expression of the intracellular STAT3 phosphorylation.