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TAZ/Wnt-β-catenin/c-MYC axis regulates cystogenesis in polycystic kidney disease

Authors
Lee, Eun JiSeo, EunjeongKim, Jin WonNam, Sun AhLee, Jong YoungJun, JaeheeOh, SuminPark, MinahJho, Eek-hoonRyu, Kyung HyunPark, Jong HoonKyun, Yong
Issue Date
Nov-2020
Publisher
National Academy of Sciences
Keywords
C-myc; Polycystic kidney; TAZ
Citation
Proceedings of the National Academy of Sciences of the United States of America, v.117, no.46, pp.29001 - 29012
Journal Title
Proceedings of the National Academy of Sciences of the United States of America
Volume
117
Number
46
Start Page
29001
End Page
29012
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/1064
DOI
10.1073/pnas.2009334117
ISSN
0027-8424
Abstract
Autosomal-dominant polycystic kidney disease (ADPKD) is the most common genetic renal disease, primarily caused by germline mutation of PKD1 or PKD2, leading to end-stage renal disease. The Hippo signaling pathway regulates organ growth and cell proliferation. Herein, we demonstrate the regulatory mechanism of cystogenesis in ADPKD by transcriptional coactivator with PDZ-binding motif (TAZ), a Hippo signaling effector. TAZ was highly expressed around the renal cyst-lining epithelial cells of Pkd1-deficient mice. Loss of Taz in Pkd1-deficient mice reduced cyst formation. In wild type, TAZ interacted with PKD1, which inactivated β-catenin. In contrast, in PKD1-deficient cells, TAZ interacted with AXIN1, thus increasing β-catenin activity. Interaction of TAZ with AXIN1 in PKD1-deficient cells resulted in nuclear accumulation of TAZ together with β-catenin, which up-regulated c-MYC expression. Our findings suggest that the PKD1–TAZ–Wnt–β-catenin–c-MYC signaling axis plays a critical role in cystogenesis and might be a potential therapeutic target against ADPKD. © 2020 National Academy of Sciences. All rights reserved.
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