大肠腺瘤性息肉病
基因
癌症研究
生物
癌基因
抑制器
连环蛋白
抑癌基因
突变
分子生物学
遗传学
结直肠癌
Wnt信号通路
癌症
细胞周期
癌变
作者
Tong‐Chuan He,Andrew B. Sparks,Carlo Rago,Heiko Hermeking,Leigh Zawel,Luís Teixeira da Costa,Patrice J. Morin,Bert Vogelstein,Kenneth W. Kinzler
出处
期刊:Science
[American Association for the Advancement of Science]
日期:1998-09-04
卷期号:281 (5382): 1509-1512
被引量:4548
标识
DOI:10.1126/science.281.5382.1509
摘要
The adenomatous polyposis coli gene (APC) is a tumor suppressor gene that is inactivated in most colorectal cancers. Mutations of APC cause aberrant accumulation of beta-catenin, which then binds T cell factor-4 (Tcf-4), causing increased transcriptional activation of unknown genes. Here, the c-MYC oncogene is identified as a target gene in this signaling pathway. Expression of c-MYC was shown to be repressed by wild-type APC and activated by beta-catenin, and these effects were mediated through Tcf-4 binding sites in the c-MYC promoter. These results provide a molecular framework for understanding the previously enigmatic overexpression of c-MYC in colorectal cancers.
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