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目的研究过氧化物酶体增殖激活受体(PPARγ)是否体外参与调节胃癌MKN45细胞VEGF mRNA的表达及临床意义。方法体外培养人胃癌细胞系MKN45,不同浓度的PPARγ激动剂(曲格列酮),PPARγ特异性抑制物体外作用细胞,EMSA测定细胞PPARγ的活性,RT-PCR检测细胞VEGF mRNA的表达。结果相对于对照组,随曲格列酮浓度的增加,胃癌MKN45细胞株PPARγ活性显著性升高(P<0.01),VEGF mRNA的表达显著性降低(P<0.01),且呈剂量依赖关系;PPARγ特异性抑制物能显著性抑制曲格列酮诱导的胃癌MKN45细胞株PPARγ的活化和VEGF mRNA的表达的下调(P<0.01)。结论PPARγ可能参与调节胃癌MKN45细胞株VEGF mRNA的表达,曲格列酮通过激活PPARγ,抑制胃癌MKN45细胞株VEGF mRNA的表达,可能为胃癌的治疗提供新的靶点。
Objective To investigate whether peroxisome proliferator - activated receptor (PPARγ) is involved in the regulation of VEGF mRNA expression in gastric cancer MKN45 cells in vitro and its clinical significance. Methods Human gastric cancer cell line MKN45, different concentrations of PPARγ agonist (troglitazone) and PPARγ specific inhibitor were used to culture in vitro. The activity of PPARγ was measured by EMSA. The expression of VEGF mRNA was detected by RT-PCR. Results Compared with the control group, the PPARγ activity of gastric cancer MKN45 cells was significantly increased (P <0.01) and the expression of VEGF mRNA was significantly decreased (P <0.01) with the increase of troglitazone concentration in a dose - dependent manner. PPARγ specific inhibitor could significantly inhibit the activation of PPARγ and the down-regulation of VEGF mRNA in troglitazone-induced gastric cancer MKN45 cells (P <0.01). Conclusion PPARγ may be involved in the regulation of VEGF mRNA expression in gastric cancer MKN45 cells. Troglitazone may be a new target for the treatment of gastric cancer by activating PPARγ and inhibiting the expression of VEGF mRNA in gastric cancer MKN45 cells.