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TAZ/Wnt-β-catenin/c-MYC axis regulates cystogenesis in polycystic kidney disease
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TAZ/Wnt-β-catenin/c-MYC axis regulates cystogenesis in polycystic kidney disease
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Journal Article
TAZ/Wnt-β-catenin/c-MYC axis regulates cystogenesis in polycystic kidney disease
2020
Overview
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.
Publisher
National Academy of Sciences
Subject
/ Cysts
/ Epithelial Cells - metabolism
/ Humans
/ Kidneys
/ Mice
/ Mutation
/ Polycystic Kidney Diseases - genetics
/ Polycystic Kidney Diseases - metabolism
/ Polycystic Kidney Diseases - pathology
/ Polycystic Kidney, Autosomal Dominant - genetics
/ Polycystic Kidney, Autosomal Dominant - metabolism
/ Polycystic Kidney, Autosomal Dominant - pathology
/ Protein Kinase C - deficiency
/ Proto-Oncogene Proteins c-myc - metabolism
/ Regulatory mechanisms (biology)
/ Trans-Activators - metabolism
/ TRPP Cation Channels - genetics
