C-erbB2与乳腺癌三苯氧胺耐药细胞生长关系的研究  

Study of Relationship between C-erbB2 and Tamoxifen-resistance in Breast Cancer

作　　者：赵文辉[1] 张清媛[1] 康欣梅[1] 

机构地区：[1]哈尔滨医科大学附属肿瘤医院,哈尔滨150040

出　　处：《现代生物医学进展》2007年第2期182-184,共3页Progress in Modern Biomedicine

基　　金：国家自然科学基金(30572136);哈尔滨医科大学附属肿瘤医院科研启动基金(JJ2005001)

摘　　要：目的:探讨获得性三苯氧胺(TAM)抵抗乳腺癌细胞的生长调节途径及三苯氧胺(TAM)获得性抵抗的发生机制。方法:TAM诱导野生型人乳腺癌细胞系MCF-7/WT构建TAM抵抗的细胞系MCF-7/TAMR,RT-PCR、Western blot及免疫细胞化学方法比较MCF-7/TAMR与MCF-7/WT细胞系中C-erbB2 mRNA、蛋白表达及其活化状态的不同,用C-erbB2单克隆抗体herceptin对两种细胞系进行干预,观察细胞生长变化。结果:与MCF-7/WT细胞相比,MCF-7/TAMR细胞中CerbB-2的mRNA增加3倍(P＜0．05)．蛋白增加1．5倍(P＜0．05)．Herceptin处理MCF-7/TAMR细胞,明显抑制了细胞的生长。结论:表皮生长因子受体特异性配体的自分泌释放作用可能通过CerbB-2/MAPK途径引起MCF-7/TAMR细胞的生长。Objective： To study the growth regulation pathway of TAM-resistant breast cancer cell and the mechanism of required TAM-resistance（TAMR）. Methods： Wild-type MCF-7/WT was induced by TAM （=Tamoxifen） to construct MCF- 7/TAMR. RT-PCR,Western blot and immuocytochemical methods were used to detect the expression of C-erbB2 mRNA and protein in wild-type MCF-7 and in TAM-R MCF-7 cell line. Herceptin was used to inhibit the growth of the two cells. Results： Compared with wild-type MCF-7 cells, the mRNA of C-erbB2 increased 3 times with the protein 1.5 times higher in TAM-R MCF-7 cells. Treatment of TAM-R cells with Herceptin blocked c-erbB receptor and strongly inhibited cell growth. Conclusion： These results demonstrate that TAM-R MCF-7 cell growth is mediated by the autocrine release and C-erbB2/MAPK pathway may increase the growth of Tamoxifen-resistant cells.

关 键 词：C—erbB2 乳腺癌 三苯氧胺 

分 类 号：R730.5[医药卫生—肿瘤]