RNA干扰成纤维细胞生长因子受体3基因对卵巢癌细胞增殖凋亡、免疫及NF-κB信号通路的影响

Effect of fibroblast growth factor receptor 3 knockdown on the proliferation and apoptosis of ovarian cancer cells,and NF-κB signaling activation

目的探讨RNA干扰成纤维细胞生长因子受体3(FGFR3)表达对卵巢癌细胞增殖凋亡、B7-H1表达及NF-κB信号通路的影响。方法采用LipofectamineTM2000将FGFR3 siRNA转染至人卵巢癌SK-OV-3细胞中,Western blotting检测细胞中FGFR3、B7-H1、p-NF-κB、p-IκB、cyclinD1和survivin蛋白的表达;CCK8检测细胞活力;流式细胞仪检测细胞凋亡率。结果转染FGFR3 siRNA可明显降低FGFR3、B7-H1、p-NF-κB、cyclinD1和survivin的蛋白表达,增加p-IκB的蛋白表达,抑制细胞活力,诱导细胞凋亡。结论RNA干扰卵巢癌FGFR3表达可降低癌细胞活力,诱导细胞凋亡,降低免疫逃逸相关基因B7-H1表达,其机制可能与下调NF-κB信号通路有关。

Objective To investigate the effect of fibroblast growth factor receptor 3(FGFR3)knockdown on the proliferation and apoptosis of ovarian cancer cells,as well as B7-H1 expression and NF-κB signaling activation.Methods FGFR3 siRNA was transfected into human ovarian cancer SK-OV-3 cells by using LipofectamineTM2000.Levels of FGFR3,B7-H1,p-NF-κB,p-IκB,cyclinD1 and survivin protein were detected by Western blotting assay.Cell activity was detected by CCK8 assay,and cell apoptosis was detected by flow cytometry.Results Levels of FGFR3,B7-H1,p-NF-κB,cyclinD1 and Survivin were significantly reduced,but p-IκB was increased.Cell viability was inhibited and cell apoptosis was increased in SK-OV-3 cells after transfection with FGFR3 siRNA.Conclusion Inhibition of FGFR3 by RNA interference in ovarian cancer can inhibit cell viability,increase cell apoptosis,with the decrease of immune escape related gene B7-H1,contributing to the inactivation of NF-κB signaling.