Rnai-Mediated DEPDC1 Depletion Inhibits Cell Migration And Invasion In Nasopharyngeal Carcinoma Cell Line HNE-1 And CNE-1

DEPDC1 is a novel tumor-relative gene and plays important roles in a variety of malignant tumors development. Our previous study indicated that DEPDC1-depletion represses cell proliferation and induces apoptosis in nasopharyngeal carcinoma cell line HNE-1.Objective: This study aims to clarify that the potential role for migration and invasion of DEPDC1 in HNE-1 and CNE-1.Methods:(1) The effect of DEPDC1 depletion on cell migration and invasion abilities in nasopharyngeal carcinoma cell lines HNE-1 and CNE-1: On the basis of principles of siRNA, DEPDC1 siRNA was designed and transfected into the cell lines HNE-1 and CNE-1. The expression of DEPDC1 gene was determined in the mRNA and protein levels. DEPDC1 proteins were located in cells by immunofluorescence, cell morphological changes were observed by inverted microscope, the migration and invasion abilities were detected by wound healing assay、transwell migration and invasion assays.(2) The mechanism of DEPDC1 depletion on cell migration and invasion abilities of HNE-1 and CNE-1: the expression of EMT-associated key molecules was tested by RT-PCR 、 Western blot and cell immunefluorescence in HNE-1 and CNE-1 cells.Results:(1) DEPDC1 depletion significantly inhibited the migration and invasion abilities in HNE-1 and CNE-1 cells using Wound healing and Transwell, respectively.(2) the expression levels of the Twist1 and Vimentin were down-regulated in DEPDC1 depletion significantly than that of control using RT-PCR、Western blot and cell immunofluorescence.Taken together, DEPDC1 depletion significantly inhibites the migration and invasion abilities in nasopharyngeal carcinoma cell lines.In summary, these findings suggest that in nasopharyngeal carcinoma cells DEPDC1 plays a key role in cell invasion and metastasis by regulating the expression of EMT-associated key molecules Twist1. It suggests that high-level expression of DEPDC1 enhance the migration and invasion activities in nasopharyngeal carcinoma, but the molecular mechanism is worth for further study.