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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HO 8910增殖过程
To investigate the molecular mechanism by which synthetic dexamethasone (Dex) can inhibit the proliferation of human ovarian cancer cell line HO 8910. RT-PCR was used to detect the expression of cyclin-dependent kinase inhibitor p2 1 WAF1, transforming growth factor β1 (TGFβ1) and its type I receptor (TβR I) and type II receptor (TβR II) The chemical method was used to analyze the protein expression level of TβR II. Dex was found to induce p2 1 WAF1 mRNA expression in HO 8910 cells. Compared with the control group, the expression of p2 1 WAF1 mRNA in 10 - 7 mol LDex treated cells increased by 844 fold (P <0.01). Dex also could upregulate the expression level of TβR II mRNA. Dex also induced the increase of TβR II protein expression after treated with 10 -7 mol LDex for 8 h, which resulted in a 12-fold increase in TβR II mRNA expression (P <0.01). These effects can be reversed by the glucocorticoid receptor (GR) antagonist RU486. However, TGFβ1 and TβR mRNA expression was not affected by Dex. The above results suggest that Dex can promote the expression of p2 1 WAF1 and TβR II through GR mediation, which may be involved in its inhibition on the proliferation of human ovarian cancer cell line HO 8910