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Transforming growth factor-β (TGF-β) induces epithelial-mesenchymal transition (EMT) primarily via a Smad‑dependent mechanism. However, there are few studies available on TGF-β-induced EMT through the activation of non‑canonical pathways. In this study, the Cdc42-interacting protein-4 (CIP4)/partitioning-defective protein 6 (Par6) pathway was investigated in TGF-β1‑stimulated NRK-52E cells. Rat NRK-52E cells were obtained and stimulated with TGF-β1. The expression levels of E-cadherin, α-smooth muscle actin (α-SMA) and CIP4 were then examined by western blot analyses. Rat NRK-52E cells were transfected with Par6 or CIP4 small interfering RNA (siRNA), and scrambled siRNA as controls. The cells were incubated with 20 ng/ml of TGF-β1 for 72 h in order to observe the effects of Par6 and CIP4 silencing. Confocal fluorescence microscopy was also applied to reveal the expression and distribution of E-cadherin, α-SMA, Par6 and CIP4. The results demonstrated that E-cadherin expression was decreased, and α-SMA expression was increased in the TGF-β1‑stimulated cells. Simultaneously, the increased expression of CIP4 and p-Par6 was confirmed by western blot analyses. The results of confocal fluorescence microscopy revealed that rat CIP4 exhibited cluster formations located adjacent to the cell periphery; however, as for the protein expression and distribution of Par6, there was no obvious difference between the control cells and cells exposed to TGF-β1. siRNA molecules capable of CIP4 and Par6 knockdown were used to demonstrate reversed TGF-β1‑induced EMT. Moreover, CIP4 loss of function reversed the increase in p-Par6 protein expression in the TGF-β1‑stimulated NRK-52E cells. A similar result was observed with the decreased CIP4 protein expression due to Par6 loss of function. Our data thus suggest that the CIP4/Par6 complex plays an important role in the occurrence of EMT in TGF-β1-stimulated NRK-52E cells. The underlying mechanisms are mediated, at least in part, through the upregulation of CIP4, which occurrs due to stimulation with TGF-β1; subsequently, CIP4 increases the phosphorylation of Par6, which accelerates the process of EMT.

Suppression of CIP4/Par6 attenuates TGF-β1-induced epithelial-mesenchymal transition in NRK-52E cells