糖皮质激素对人卵巢癌HO-8910细胞TβR-Ⅱ的上调作用  

Up-regulation of TβR-Ⅱ by Glucocorticoid in Human Ovarian Cancer HO-8910 Cells

作　　者：夏冰[1] 卢建[2] 王钢[2] 

机构地区：[1]广州军区广州总医院,510010 [2]上海第二军医大学病理生理学教研室,200433

出　　处：《实用癌症杂志》2002年第5期452-454,共3页The Practical Journal of Cancer

摘　　要：目的　研究转化生长因子 -β1(TGF -β1)通路 ,是否参与人工合成的糖皮质激素地塞米松 (Dex)对人卵巢癌细胞系HO -8910的增殖抑制过程。方法　分别采用细胞计数和流式细胞分析方法检测细胞增殖和细胞周期分布 ;采用定量RT -PCR、酶联免疫吸附法 (ELISA)和 (或 )免疫细胞化学法 ,检测TGF -β1及其I型受体 (TβR -Ⅰ )和Ⅱ型受体 (TβR -Ⅱ )的表达水平。 结果　Dex可引起HO -8910细胞周期G0 G1 期进展停滞 ,并可明显上调TβR -ⅡmRNA的表达 ,且具有浓度依赖性特点 ,Dex作用HO -8910细胞 8h时作用最强 ,此时 10 - 7mol LDex组TβR -ⅡmRNA水平比对照组高 1.4倍 (P <0 .0 1) ;相应地 ,TβR -Ⅱ的蛋白表达水平也增高 ,糖皮质激素受体 (GR)阻断剂RU 486能够逆转这些作用 ,而Dex对TGF -β1和TβR -ⅠmRNA的表达无调节作用。结论　Dex抑制HO -8910细胞增殖的机制可能包括上调TβR -Ⅱ的表达 。Objective To investigate whether transforming growth factor β1(TGF β1) pathway is involved in the mechanism of dexamethasone(Dex) mediated proliferation inhibition in ovarian cancer cell line HO 8910.Methods To analyse cell proliferation and cell cycle distribution by cell counts and flow cytometric analysis,respectively;to determine the expression levels of TGF β1,TGF β receptor Ⅰ(TβR Ⅰ) and receptor Ⅱ(TβR Ⅱ) by quantative RT PCR,ELISA and/or immunocytochemistry methods.Results Dex induced a G 0/G 1 cell cycle arrest in HO 8910 cells,and it up regulated TβR Ⅱ expression in a concentration dependent manner.The level of TβR Ⅱ mRNA was the highest after treatment with Dex for 8 h,with 1.4 fold more than that of control at concentration of 10 -7 mol/L( P <0.01).The expression of TβR Ⅱ protein was also enhanced.RU486,an antagonist of glucocorticoid receptor,could reverse these effects.Besides,Dex didn′t affect the expression of TGF β1 or TβR Ⅰ mRNA.Conclusion Up regulation of TβR Ⅱ mediated by GR might take part in the course of Dex induced inhibition of HO 8910 cell proliferation.

关 键 词：糖皮质激素 转化生长因子 受体 卵巢癌细胞系 细胞增殖 流式细胞术 

分 类 号：R737.31[医药卫生—肿瘤] R977.1[医药卫生—临床医学]