Research On TGF-beta1Induced Epithelial To Mesenchymal Transition Of Nasopharyngeal Carcinoma Cells

Objective Nasopharyngeal carcinoma(NPC) is a common cancer of the head andneck cancer in Southern China, and the major cause of death for nasopharyngealcarcinoma patients are caused by metastasis. It has been proven thatepithelial-mesenchymal transition(EMT) could promote tumor invasion andmetastasis.Transforming growth factor beta-1(TGF-β1) has been identified as themain inducer of EMT. The aim of this study was to examine whether TGF-β1couldinduce EMT in the human nasopharyngeal carcinoma cell line, CNE-1, and toinvestigate the influence of TGF-β1on mobile and invasive ability of CNE-1.Methods Cultured human nasopharyngeal carcinoma cell line, CNE-1, werestimulated with10ng/mL TGF-beta1. The morphologic changes were observedunder phase-contrast microscopy; The epithelial cell marker E-cadherin,mesenchymal cell maker N-cadherin and transcription factor Slug were detectedusing Western blot, immunoflurescence staining and RT-PCR. In addition, themigration and invasion mobility were examined by wound-healing and transwellinvasion assay.Results After TGF-beta1stimulation, human nasopharyngeal carcinoma cell line,CNE-1, were converted from a "cobblestone" epithelial structure into an elongatedspindle-like shape under phase-contrast microscopy. Proteomic and genomic analyses suggested that TGF-beta1downregulate the expression of epithelial makerprotein E-cadherin and upregulate the expression of mesenchymal maker proteinN-cadherin and transcription factor Slug. Moreover, wound-healing and transwellinvasion assay indicated that TGF-beta1promoted CNE-1cell migration andinvasion mobility dramatically.Conclusions This study demonstrates that TGF-beta1could induce EMT in the NPCcell line, CNE-1, and contribute to migration and invasion mobility.