上皮调节蛋白对表皮癌细胞A431生长的抑制机制  

On the Mechanism of Growth Inhibition of Epiregulin in A431 Epidermal Carcinoma Cells

作　　者：席全胜[1] 潘巍[1] 张倩[1] 钱欣国[1] 李载平[1] 甘人宝[1] 

机构地区：[1]中国科学院上海生物化学研究所,上海200031

出　　处：《生物化学与生物物理学报》2000年第6期601-604,共4页

摘　　要：对重组蛋白上皮调节蛋白 (epiregulin ,EPI)抑制表皮癌细胞A4 3 1的生长机制进行了初步的探讨。通过Northern杂交发现 ,细胞受到重组蛋白质刺激后 ,其周期蛋白激酶的抑制因子 p2 1WAF1/CIP1的mRNA含量有较明显的提高。报告基因分析表明 ,p2 1WAF1/CIP1启动子区的转录因子STAT1结合序列对EPI的刺激有较强的反应。流式细胞仪的测定则表明 ,在EPI导致的细胞生长抑制中并没有凋亡的发生。以上结果表明 :EPI对A4 3 1细胞生长抑制可能是通过转录因子STAT1介导的增强p2 1WAF1/CIP1表达 。Preliminary investigation on the mechanism of the gr owth inhibition by recombinant epiregulin(EPI)of epidermal carcinoma cell A431 i s reported. Northern blotting indicated that the mRNA level of cyclin dependent kinase(CDK)inhibitor, p21 WAF1/CIP1 , was increased significantly after stim ulation of the recombinant epiregulin protein. Luc reporter revealed that STAT1 could bind the promoter region of p21 in response to the EPI signal. Flow cytome try assay showed that the EPI induced growth inhibition was not related to the apoptosis. The above results indicate that the EPI induced cell growth inhibiti on might result from the STAT1 stimulated expression of p21, leading to the G1 arrest.

关 键 词：生长抑制 STAT1 凋亡 表皮癌细胞 

分 类 号：Q519.2[生物学—生物化学]