UNC119 promotes the malignant progression of nasopharyn- geal carcinoma cells by regulating Wnt/β-catenin pathway

UNC119, also known as human retinal gene 4 (HRG4), has been found to contribute to the tumorigenesis of hepatocellular carcinoma. However, the role and mechanism of UNC119 in nasopharyngeal carcinoma has not been systematically investigated yet. Data from western blot and RT-qPCR assays showed that UNC119 was elevated in nasopharyngeal carcinoma cells and tissues. Functional assays demonstrated that transfection with siRNA targeting UNC119 reduced cell viability and suppressed proliferation, invasion, and migration of nasopharyngeal carcinoma cells. Moreover, silence of UNC119 decreased the protein expressions of N-cadherin and vimentin while, on the other hand, increased the protein expressions of E-cadherin and zonula occludes-1 (ZO-1) to suppress epithelial-mesenchymal transition in nasopharyngeal carcinoma. The protein expressions of Axin2 and adenomatous polyposis coli (APC) were up-regulated, while ??-catenin and matrix metalloproteinase-7 (MMP-7) were down-regulated by silence of UNC119 in nasopharyngeal carcinoma cells. In conclusion, knockdown of UNC119 suppressed cell growth and metastasis, and repressed epithelial-mesenchymal transition in nasopharyngeal carcinoma through inactivation of Wnt/??-catenin pathway.

Automated summary

UNC119 plays a role in the tumorigenesis of nasopharyngeal carcinoma by promoting cell proliferation, invasion, and migration, as well as epithelial-mesenchymal transition. Knockdown of UNC119 suppresses cell growth and metastasis in nasopharyngeal carcinoma by inhibiting the activation of the Wnt/β-catenin pathway.