KCNIP3 silence promotes proliferation and epithelial-mesenchymal transition of papillary thyroid carcinoma through activating Wnt/β-catenin pathway

Purpose: Papillary thyroid carcinoma (PTC) is the common endocrine malignancy. Kv channel interacting protein 3 (KCNIP3) has been investigated in a variety of diseases, but its role and underlying mechanism in PTC are not fully delineated. Based on this, this study mainly explored the possible mechanism of KCNIP3 in PTC. Methods: KCNIP3 expression in PTC tissues was analyzed by ENCORI and validated by quantitative real-time PCR (qRT-PCR). KCNIP3 overexpression (oe-KCNIP3) or KCNIP3 silence (si-KCNIP3) was transfected into IHH4 and FTC-133 cells, respectively. Then cell biological behaviors were detected by cell function assays. The expressions of epithelial-mesenchymal transition (EMT)- and Wnt/beta-catenin pathway-related proteins were quantified by qRT-PCR and western blot. Lastly, IHH4 cells were treated with LiCl and the above assays were performed again. Results: The expression of KCNIP3 was decreased in PTC. After transfection, oe-KCNIP3 inhibited the PTC cell viability, cloning, migration and invasion but promoted apoptosis, and meanwhile, oe-KCNIP3 reduced the EMT and Wnt pathway activation. In contrast, si-KCNIP3 had the opposite effect. Moreover, LiCl, a Wnt signaling pathway activator, could reverse the above effects of oe-KCNIP3. Conclusion: KCNIP3 might play an anticarcinogenic role in PTC via inhibiting the activation of Wnt/beta-catenin signaling pathway.