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作 者:孔丽[1] 姚树坤 马英[1] 王容琦[1] 张玉果[1]
机构地区:[1]河北医科大学第三医院肝病科,河北石家庄050051 [2]第四医院消化科,河北石家庄050050
出 处:《临床肝胆病杂志》2007年第4期270-273,共4页Journal of Clinical Hepatology
基 金:河北省自然科学基金资助(303516)
摘 要:探讨TGFβ1/Smads信号转导通路的改变在原发性肝癌发病机制中的作用。应用western blotting法和RT-PCR法对肝癌组织TGFβ受体Ⅰ、TGFβ受体Ⅱ、Smad2,Smad4,Smad7蛋白和mRNA水平进行检测,并与正常肝组织和癌旁组织比较。结果显示肝癌组织TGFβRⅡ、Smad4 mRNA和蛋白表达较正常及癌旁组织显著降低,Smad7 mRNA和蛋白表达、Smad7/Smad4比值显著升高。提示TGFβ1/smads信号转导通路被抑制,使TGFβ1介导的抗增殖信号不能正常下传,可能是肝癌发生的机制之一。To explore the effect of alteration of TGFβⅠ/Smads signaling pathway on pathogenesis of HCC. The expression in protein level and mRNA level of TGFβⅠ , TGFβⅡ, Smad2, Smad4 and Smad7 in HCC liver tissues were detected by western blotting asssays and RT- PCR assays, and compared with normal liver control tissue and adjacent nonneoplastic tissues. The expression of TGFβⅡ and Smad4 mRNA in HCC liver tissues were significantly lower than that in normal control liver and adjacent nonneoplastic tissues. The expression of Smad7 mRNA and the ratio of SmadT/Smad4 in HCC liver were significantly higher than that in normal control liver and adjacent nonneoplastic liver tissues. The tendency of protein expression of TGFβⅡ , Smad4 and Smad7 were similar to mRNA expression in HCC liver tissues. If the TGFβⅠ/Smads signaling pathway was repressed, the information of growth inhibition could not be transmitted. It might be one of the factors of HCC pathogenesis.
关 键 词:原发性肝癌 肝组织 TGFΒ受体 SMADS TGFβ1/Smads信号通路
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