期刊论文详细信息
Journal of Ovarian Research
The effects of dexamethasone on the proliferation and apoptosis of human ovarian cancer cells induced by paclitaxel
Rong Zhang1  Yuhong Han1  Qian Dong1  Huan Lu1  Jianhua Guan1  Wenjing Hou1 
[1] Department of Obstetrics and Gynecology, Shanghai Jiaotong University-Affiliated Sixth People’s Hospital of Fengxian Branch, 6600 Nanfeng Road, Shanghai 201499, People’s Republic of China
关键词: Survivin;    Paclitaxel;    Ovarian cancer;    Dexamethasone;    Cleaved caspase-3;    Bcl-XL;   
Others  :  1133157
DOI  :  10.1186/s13048-014-0089-z
 received in 2014-05-30, accepted in 2014-08-31,  发布年份 2014
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【 摘 要 】

Background

Dexamethasone (DEX) has been routinely used as a pre-treatment in the clinical application of paclitaxel (PTX) to treat ovarian cancer. However, PTX-induced apoptosis might be inhibited by DEX. This study was undertaken to investigate the effects of DEX on the apoptosis induced by PTX.

Methods

Both of SKOV-3 and HO-8910 human ovarian cancer cells were divided into four groups: (1) untreated (Con); (2) treated with DEX (0.1 μM) alone; (3) treated with PTX (50 nM); and (4) pre-treated with DEX (0.1 μM), and 24 h later, treated with PTX (DEX + PTX). Cell proliferation was determined by the 3-(4,5)-dimethylthiahiazo (−z-y1)-3,5-di- phenytetrazoliumromide (MTT) dye uptake method, while cell apoptosis was analyzed by propidium iodide (PI) staining and flow cytometry. Then, reverse transcription polymerase chain reactions (RT-PCRs) were applied to semi-quantitative analysis, followed by western blot analysis. Statistical analysis was performed, with Fisher’s least significant difference test.

Results

Our results demonstrated that DEX can differentially inhibit SKOV-3 and HO-8910 cell proliferation induced by PTX and decrease the apoptosis rates in cancer cells. Pre-treatment with DEX could up-regulate the expressions of members of anti-apoptotic Bcl-2 family (Bcl-2 and Bcl-XL) and members of IAP family (survivin). The expression of cleaved caspase-3 was down-regulated by DEX, shown by semi-quantitative RT-PCRs and western blot analysis.

Conclusions

Our data gained invaluable insights of the antagonistic mechanisms of DEX on PTX-induced cancer cell death and may provide new methods of using DEX as antineoplastic drugs or agents in the clinical treatment for ovarian cancer patients.

【 授权许可】

   
2014 Hou et al.; licensee BioMed Central Ltd.

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