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

•KCNIP3 expression was down-regulated in PTC.•KCNIP3 overexpression inhibited the PTC malignant phenotype while KCNIP3 silence promoted it.•KCNIP3 overexpression suppressed EMT and Wnt/β-catenin signaling pathway activation.•LiCl reversed the effect of oe-KCNIP3 on PTC cell biological behaviors, EMT and Wnt/β-catenin pathway. 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. 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/β-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. 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. KCNIP3 might play an anticarcinogenic role in PTC via inhibiting the activation of Wnt/β-catenin signaling pathway.