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

Abstract

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 β-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/β-catenin pathway.

Elevated expression of EAPP is associated with poor prognosis and promotes tumor progression in epithelial ovarian cancer

“…EMT is a well-defined process that promotes tumor cell migration [17][18][19][20]. In this study, we discovered that EAPP overexpression promoted EMT by decreasing the expression of the mesenchymal markers, Vimentin, Snail, and Slug by upregulating the epithelial marker E-cadherin.…”