Cystic renal neoplasia following conditional inactivation of Apc in mouse renal tubular epithelium

被引:112
作者
Qian, CN
Knol, J
Igarashi, P
Lin, FM
Zylstra, U
Teh, BT
Williams, BO
机构
[1] Van Andel Res Inst, Lab Cell Signaling & Carcinogenesis, Grand Rapids, MI 49503 USA
[2] Van Andel Res Inst, Canc Genet Lab, Grand Rapids, MI 49503 USA
[3] Univ Texas, SW Med Ctr, Dept Internal Med, Dallas, TX 75390 USA
[4] Univ Texas, SW Med Ctr, Dept Pediat, Dallas, TX 75390 USA
[5] Univ Texas, SW Med Ctr, Div Basic Sci, Dallas, TX 75390 USA
[6] Calvin Coll, Dept Biol, Grand Rapids, MI 49546 USA
关键词
D O I
10.1074/jbc.M410697200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alterations in Wnt/beta-catenin signaling have been linked to abnormal kidney development and tumorigenesis. To gain more insights into the effects of these alterations, we created mice carrying a conditional deletion of the Apc tumor suppressor gene specifically in the renal epithelium. As expected, the loss of Apc leads to increased levels of beta-catenin protein in renal epithelium. Most of these mice die shortly after birth, and multiple kidney cysts were found upon, histological. examination. Only rarely did these animals survive to adulthood. Analysis of these adults revealed severely cystic kidneys associated with the presence of renal adenomas. Our results confirm an important role for proper regulation of Wnt/beta-catenin signaling in renal development and provide evidence that dysregulation of the pathway can initiate tumorigenesis in the kidney.
引用
收藏
页码:3938 / 3945
页数:8
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