高转移肝癌MHCC97细胞中JAK/STATs通路相关分子表达的研究  

The expression of several molecules in JAK/STATs signaling pathway in MHCC97 hepatocellular carcinoma cells with high metastatic potential

作　　者：吴伟忠[1] 孙惠川[1] 高艳琴[2] 王鲁[1] 汤钊猷[1] 刘康达[1] 

机构地区：[1]复旦大学中山医院肝癌研究所肿瘤血管实验室,上海200032 [2]复旦大学医学神经生物学国家重点实验室,上海200032

出　　处：《肿瘤》2007年第1期1-4,共4页Tumor

基　　金：国家自然科学基金资助项目(编号:30300400)

摘　　要：目的:干扰素α能明显抑制裸鼠MHCC97肝癌移植瘤的生长,但对该细胞的增殖无影响。本研究着重探讨导致MHCC97细胞对干扰素α无应答的分子机理。方法:用RT-PCR、免疫印迹及核苷酸测序等方法研究MHCC97细胞中JAK/STATs通路上干扰素α受体、irf9、stat1及stat2基因的转录和蛋白的表达。结果:MHCC97细胞构成性转录和翻译stat1、stat2分子;虽同时转录一定量的irf9mRNA,但检测不到相应的蛋白;测序分析发现irf9基因的核苷酸组成存在几个点突变。结论:由irf9基因突变所引起的JAK/STATs信号转导功能的不完整,可能是该细胞对干扰素α增殖抑制无应答的分子原因之一。Objective： Interferon apha（IFN-α） ha significatly inhibitory effects on the MHCC97 trasplated tumor growth in nude mice, but ha no effect on the proliferaion of MHCC97 cells. In this study we try to elucidae the molecula mechaisms for non-response of MHCC97 cells to IFN-α in vitro. Methods：The mRNA ad protein expressions of severa molecules （IFN -α receptor, irfg, stal ad sta2） in the Jaus kinae （JAK）/ signa trasducer ad atuaor of trascription （STATs） signaing pahwa were determined by reverse trascriptae-polymerae chan reation, western blotting, ad cDNA sequence aaysis in MHCC97 cells. Results： MHCC97 cells constitutively expressed the mRNAs of stal ad sta2 a well a traslaed their corresponding proteins. Although the cells expressed alower level of irf9 mRNA,irf9 protein wa not detected. Sequence aaysis showed tha the nucleotides of Jr f9 gene ha severa point mutaions. Conclusion： Functiona deficiency of JAK/STATs signaing pahwa results from it f9 gene mutaions,which might be one of the molecula mechaisms for the nonresponse of MHCC97 cells on IFN-α treament.

关 键 词：癌 肝细胞 干扰素Α 信号传递 基因表达调控 肿瘤 MHCC97细胞 

分 类 号：R735.7[医药卫生—肿瘤]