Wnt Signaling Stimulates Transcriptional Outcome of the Hedgehog Pathway by Stabilizing GLI1 mRNA

被引：96
|
作者：
Noubissi, Felicite K. [1 ]
Goswami, Srikanta [1 ]
Sanek, Nicholas A. [2 ]
Kawakami, Kazuyuki [5 ]
Minamoto, Toshinari [5 ]
Moser, Amy [3 ,4 ]
Grinblat, Yevgenya [2 ]
Spiegelman, Vladimir S. [1 ,4 ]
机构：
[1] Univ Wisconsin, Dept Dermatol, Sch Med & Publ Hlth, Madison, WI 53706 USA
[2] Univ Wisconsin, Dept Zool & Anat, Sch Med & Publ Hlth, Madison, WI 53706 USA
[3] Univ Wisconsin, Dept Human Oncol, Sch Med & Publ Hlth, Madison, WI 53706 USA
[4] Univ Wisconsin, Paul P Carbone Comprehens Canc Ctr, Sch Med & Publ Hlth, Madison, WI 53706 USA
[5] Kanazawa Univ, Canc Res Inst, Kanazawa, Ishikawa 920, Japan
来源：
CANCER RESEARCH | 2009年 / 69卷 / 22期
关键词：
UBIQUITIN LIGASE RECEPTOR; BETA-CATENIN; C-MYC; COLORECTAL-CANCER; SONIC HEDGEHOG; CODING REGION; CELLS; SHH; EXPRESSION; ZEBRAFISH;
D O I：
10.1158/0008-5472.CAN-09-1500
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Writ and Hedgehog signaling pathways play central roles in embryogenesis, stem cell maintenance, and tumorigenesis. However, the mechanisms by which these two pathways interact are not well understood. Here, we identified a novel mechanism by which Writ signaling pathway stimulates the transcriptional output of Hedgehog signaling. Wnt/beta-catenin signaling induces expression of an RNA-binding protein, CRD-BP, which in turn binds and stabilizes GLI1 mRNA, causing an elevation of GLI1 expression and transcriptional activity. The newly described mode of regulation of GLI1 seems to be important to several functions of Writ, including survival and proliferation of colorectal cancer cells. [Cancer Iles 2009;69(22):8572-8]
引用
收藏
页码：8572 / 8578
页数：7
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