Enhanced renal c-Myc-induced ADPKD in SBM transgenic mice lead conversely to striking upregulation of Pkd1/Pc1 expression and β-catenin activation, lending credence for reciprocal crosstalk between c-Myc and Pc1.
Pharmacologically inhibiting β-catenin stability or the production of mature Wnt protein, or genetically reducing the expression of Ctnnb1 (which encodes β-catenin), suppressed the formation of renal cysts, improved renal function, and extended survival in ADPKD mice.
Levels of NHERF1 protein and mRNA were significantly lower, and β-catenin levels significantly higher, in patients with ADPKD and Han:SPRD (cy/+) rats, compared with control subjects and (+/+) rats, respectively.