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HGF经HGF/Akt通路抑制肝癌细胞HCCC-9810的增殖
引用本文:王广洲,周 林,吴银霞.HGF经HGF/Akt通路抑制肝癌细胞HCCC-9810的增殖[J].南京医科大学学报,2014(7):870-874.
作者姓名:王广洲  周 林  吴银霞
作者单位:苏北人民医院临床医学检测中心,江苏 扬州 225001;苏北人民医院临床医学检测中心,江苏 扬州 225001;苏北人民医院肿瘤科,江苏 扬州 225001
基金项目:江苏省苏北人民医院院级科研基金项目(yzucms201318)
摘    要:目的:观察肝细胞生长因子(HGF)对人胆管细胞型肝癌细胞HCCC-9810增殖的影响,并探讨其分子机制?方法:HGF处理HCCC-9810细胞后,用MTT及EdU法检测癌细胞的增殖;siRNA干扰技术抑制HCCC-9810细胞内源性Akt的表达,Western blot检测癌细胞Cyclin D1蛋白表达和Akt磷酸化的变化?结果:50和100 ng/ml HGF显著抑制肝癌细胞HCCC-9810的增殖?Western blot结果显示,HGF处理后的肝癌细胞Akt磷酸化和Cyclin D1表达量明显下调?siRNA干扰Akt的表达,阻断了HGF诱导的Cyclin D1表达量的下调及细胞增殖抑制?结论:HGF通过下调Akt磷酸化和Cyclin D1表达量抑制肝癌细胞HCCC-9810的增殖?

关 键 词:HGF  肝癌细胞  增殖  Akt  Cyclin  D1
收稿时间:2013/12/10 0:00:00

HGF inhibited the proliferation of liver carcinoma cell line HCCC-9810 via HGF/Akt signaling pathway
Wang Guangzhou,Zhou Lin and Wu Yinxia.HGF inhibited the proliferation of liver carcinoma cell line HCCC-9810 via HGF/Akt signaling pathway[J].Acta Universitatis Medicinalis Nanjing,2014(7):870-874.
Authors:Wang Guangzhou  Zhou Lin and Wu Yinxia
Abstract:Objective:To identify the novel function of hepatocyte growth factor (HGF) in liver carcinoma cell HCCC-9810 proliferation and the underlying molecular mechanism. Methods:The proliferation of HCCC-9810 treated with HGF was detected by MTT assay and EdU assay. The expression of Akt in HCCC-9810 cells was inhibited by siRNA. Western blot was used to detect the expression of cyclin D1 and the phosphorylation level of Akt. Results:Both 50 ng/ml and 100 ng/ml HGF significantly inhibited the proliferation of HCCC-9810. Western blotting assay showed that HGF downregulated the expression of cyclin D1 and the phosphorylation level of Akt in HCCC-9810 cells. Conclusion:These results suggest that HGF inhibited the proliferation of HCCC-9810 by suppressing the expression of cyclin D1 and the phosphorylation level of Akt. SiRNA interfered the expression of Akt,and blocked HGF-induced downregulation of cyclin D1 expression and inhibition of cell proliferation.
Keywords:HGF  liver carcinoma cell  proliferation  Akt  Cyclin D1
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