地塞米松促进卵巢癌细胞系p21/WAF1和TβR-II的表达  

Increased p21/WAF1 and TβR-II expression in an ovarian cancer cell line HO-8910 by dexamethasone

作　　者：夏冰[1] 卢建[1] 

机构地区：[1]第二军医大学病理生理学教研室,上海200433

出　　处：《基础医学与临床》2003年第4期416-419,共4页Basic and Clinical Medicine

摘　　要：探讨人工合成糖皮质激素地塞米松 (Dex)抑制人卵巢癌细胞系HO 8910增殖的分子机理。采用RT PCR测定细胞周期蛋白依赖性激酶抑制剂p2 1 WAF1,转化生长因子 β1 (TGF β1 )及其I型受体 (TβR I)和II型受体 (TβR II)的mRNA表达水平 ,免疫细胞化学方法分析TβR II的蛋白表达水平。发现Dex能够诱导HO 8910细胞p2 1 WAF1mR NA的表达 ,10 - 7mol LDex处理细胞 8h组比对照组p2 1 WAF1mRNA表达增加 2 84倍 (P <0 0 1)。并且证明Dex亦可上调TβR IImRNA的表达水平 ,10 - 7mol LDex处理 8h使TβR IImRNA的表达量比对照升高 1 2倍 (P <0 0 1) ;Dex也引起TβR II蛋白表达的增加。这些效应均可被糖皮质激素受体 (GR)拮抗剂RU4 86逆转。而TGF β1 和TβR ImRNA的表达不受Dex的影响。以上结果提示 ,Dex通过GR介导而促进p2 1 WAF1和TβR II的表达 ,可能参与其抑制人卵巢癌细胞HOTo investigate the growth inhibitory effect of dexamethasone (Dex) on human ovarian cancer cell line HO 8910. RT PCR was used to examine the mRNA expression of a cyclin dependent kinase inhibitor p21/WAF1, transforming growth factor beta1(TGF β 1), TGF β 1 receptor I(TβR I) and receptor II(TβR II ), cytoimmunochemistry method was used to assess the protein expression of TβR II. Dex increased the expression of p21/WAF1 mRNA, the level was 2.84 fold higher than the control after treatment of 8 h with 10 -7 mol/L Dex ( P <0.01).The expression of TβR II mRNA was also up regulated by Dex,which was 1.2 fold higher than control after treatment of 8 h with 10 -7 mol/L Dex ( P <0.01). Cytoimmunochemistry test showed that the expression of TβR II protein was also increased by Dex. The glucocorticoid receptor (GR) antagonist RU486 reversed these effects of Dex on HO 8910 cells. The expression of TGF β 1 or TβR I mRNA was not affected by Dex. The results suggested that Dex was able to increase the expression of both p21/WAF1 and TβR II through GR, which might play a role in the Dex induced inhibition of HO 8910 cell proliferation.

关 键 词：地塞米松 卵巢癌 细胞系 p21/WAFl TβR-Ⅱ 转化生长因子-Β1 

分 类 号：R737.31[医药卫生—肿瘤]