南方医科大学学报 ›› 2015, Vol. 35 ›› Issue (01): 88-.

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顺铂上调STAT1蛋白抑制宫颈癌细胞增殖

雷瑞霖,肖松舒,薛敏   

  • 出版日期:2015-01-20 发布日期:2015-01-20

Cisplatin inhibits proliferation of cervical carcinoma cell line by up-regulating Stat1
expression

  • Online:2015-01-20 Published:2015-01-20

摘要: 目的研究Stat1蛋白对宫颈癌Hela细胞生长、增殖及顺铂敏感性的影响及其作用机制。方法采用蛋白印迹法(Western
blot)检测不同浓度DDP处理Hela细胞后Stat1蛋白表达差异;转染Stat1-siRNA后,通过Western blot验证干扰效果;应用四甲
基偶氮唑蓝(MTT)法和5-溴脱氧尿嘧啶核苷(BrdU)观察转染Stat1-siRNA后Hela细胞对DDP敏感性变化,并检测Stat1相关细
胞因子c-Myc的表达变化。结果随着DDP浓度的增加,Hela细胞中Stat1蛋白的表达量逐渐增加,DDP浓度为5 mg/L时,Stat1
蛋白表达上调1.5倍,DDP浓度为10 mg/L时,Stat1蛋白表达上调近2倍;特异性Stat1-siRNA 使Hela细胞中Stat1的表达下调
70%,促进细胞生长和增殖;Stat1-siRNA可以降低DDP对Hela细胞生长和增殖的抑制效应,削弱DDP对c-Myc的抑制作用。
结论Hela细胞中c-Myc是STAT1发挥抑癌作用的靶点基因之一;STAT1/c-Myc通路介导了DDP抑制Hela细胞生长、增殖的作
用;STAT1可增强Hela细胞对DDP的敏感性。

Abstract: Objective To investigate the role of Stat1 gene in the proliferation and chemotherapeutic sensitivity of cervical
cancer HeLa cells. Methods The protein expression of Stat1 in the Hela cells exposed to gradient concentrations of cisplatin
(DDP) was detected by Western blotting with or without small interfering RNA (siRNA)-mediated Stat1 gene silencing. The
effect of Sata1 silencing on the sensitivity to DDP and cell proliferation of the cells was tested using MTT assay and BrdU assay,
and the expression of c-Myc was detected by Western blotting in the cells treated with siRNA and DDP. Results The expression
of Stat1 in Hela cells exposed to DDP increased with the DDP concentrations, reaching 1.5 folds of the baseline at a DDP
concentration of 5 mg/L and 2 folds at 10 mg/L. Stat1-siRNA effectively reduced Stat1 expression in Hela cells, promoted the
cell proliferation, and enhanced the expression of c-Myc; DDP inhibited the cell growth and down-regulated c-Myc expression.
Stat1-siRNA rescued DDP-induced inhibition of cell growth and c-Myc down-regulation. Conclusion The expression of Stat1
is associated with DDP sensitivity in cervical cancer cells, and Stat1 silencing can increase the sensitivity to DDP and c-Myc
expression of the cells.