吡格列酮对人胃癌细胞MCG-803生长及基因表达的影响

Influence of pioglitazone on the proliferation and apoptosis of MCG-803 human gastric cancer cell line

目的探讨过氧化物酶体增殖物激活受体γ(PPARγ)配体吡格列酮对人胃癌细胞株MCG-803生长及基因表达的影响。方法不同浓度吡格列酮作用于MCG-803后,分别应用四甲基偶氮唑盐比色法(MTT)、Annexin V/PI双染色流式细胞术、荧光定量PCR法(RT-PCR)检测细胞增殖状态、细胞凋亡率及PPARγ基因表达水平。结果不同浓度吡格列酮均可显著抑制MCG-803细胞增殖(P<0.01),且呈时间、剂量依赖性;48小时后细胞凋亡率较对照组显著增加(P<0.01);随着吡格列酮浓度增加,PPARγ基因表达呈升高趋势。结论吡格列酮呈剂量及时间依赖性抑制人胃癌细胞株MCG-803生长,并促进其凋亡;PPARγ在MCG-803中有表达且随着吡格列酮浓度增加表达上调。

Objective To investigate the influence of peroxisome proliferator-aetivated receptor γ ligand, pioglitazone, on the proliferation and apoptosis of MCG-803 gastric cancer cell line, and to examine the mRNA expression of PPARγ in MCG-803 gastric cancer cell line. Methods Cultured MCG-803 cell line were treated with pioglitazone at different concentrations respectively. MTI＂ assay and flow cytometry were used to measure the proliferation and apoptosis. RT-PCR analysis was performed to measure the level of PPARγ mRNA expression at different concentrations in MCG-803 cell line. Results PPARγ ligand pioglitazone inhibited the cell proliferation in a dose and time dependent manner compared to controls （ P 〈 0.01 ）. Flow cytometry demonstrated a significant increase of annexin V-positive cells after treatment with pioglitazone. Pioglitazone induced apoptosis in a dose dependent manner compared to controls （ P 〈 0. 01 ）. PPAR3,mRNA was expressed in human gastric cancer cell line MCG-803 and resulted in an up-regulation. Conclusion These results suggest that PPARγ ligand, pioglitazone, may inhibit the proliferation and induce apoptosis of gastric cancer cell lines. It is likely to be a useful therapeutic agent for the treatment of gastric cancer.