Claudin1 promotes the proliferation, invasion and migration of nasopharyngeal carcinoma cells by upregulating the expression and nuclear entry of β-catenin

The aim of the present study was to measure the expression of Claudin (CLDN) 1 in nasopharyngeal carcinoma (NPC) and to determine its biological function and mechanism of action. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to measure the expression of CLDN1 mRNA and protein, respectively, in the immortalized human nasopharyngeal epithelial cell line NP69 and NPC-TW01 cells. Subsequently, small interfering RNA against CLDN1 and the LV-GFP-PURO-CLDN1 lentivirus were transfected into NPC-TW01 cells. Western blotting was used to determine the effects of CLDN1 down- and upregulation on the expression of the epithelial mesenchymal transition (EMT) markers E-cadherin and vimentin. In addition, the effect of CLDN1 on the expression of β-Catenin was determined. The results demonstrated that levels of CLDN1 mRNA and protein in NPC cells were significantly higher than in NP69 cells. Furthermore, the downregulation of CLDN1 inhibited the proliferation, invasion and migration of NPC-TW01 cells. The results of western blotting demonstrated that the downregulation of CLDN1 resulted in the upregulation of E-cadherin and inhibition of vimentin in NPC-TW01 cells. By contrast, the overexpression of CLDN1 resulted in the downregulation of E-cadherin and upregulation of vimentin in NPC-TW01 cells. The downregulation of β-catenin attenuated the cancer-promoting effect of CLDN1 on NPC-TW01 cells, whereas the upregulation of β-catenin reversed the tumor-suppressing effect of CLDN1 downregulation on NPC-TW01 cells. The results of the present study therefore demonstrate that CLDN1 expression is elevated in NPC cells. As an oncogene, CLDN1 promotes the proliferation, invasion and migration of NPC cells by upregulating the expression and nuclear entry of β-catenin.