BackgroundIt has been reported that ribophorin II (RPN2) expression is increased in many cancers, but the role of RPN2 in nasopharyngeal carcinoma (NPC) remains unclear.Patients and methodsThis study found that the expression of RPN2 is increased dramatically in NPC tissues of patients compared with that in the adjacent normal tissues. This study attempted at understanding the effect of siRNA-RPN2 treatment on the migration and invasion of NPC cell lines CNE2 and HNE1.ResultsRT-PCR and Western blotting showed that RPN2 was highly expressed in CNE2 and HNE1 cells. siRNA-RPN2 treatment significantly inhibited cell viability at 24 and 48 h compared with the control group. Results of the transwell assay showed that, compared to the control groups, migration and invasion of the cells treated with siRNA-RPN2 decreased markedly. In addition, compared to the control groups, caspase-3, caspase-9, and E-cadherin expression levels increased and MMP 2 expression decreased significantly in the siRNA-RPN2-treated group. Phosphorylation of AKT and PI3K was also inhibited after siRNA-RPN2 treatment.ConclusionsiRNA-RPN2 can effectively inhibit the invasion and migration of human NPC cells via AKT/PI3K signaling. This can serve as a novel strategy for NPC treatment.
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.
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