RNAi-induced K-Ras Gene Silencing Suppresses Growth of EC9706 Cells and Enhances Chemotherapy Sensitivity of Esophageal Cancer


To analyze the growth, proliferation, apoptosis, invasiveness and chemotherapy sensitivity of EC9706 cellsafter K-Ras gene silencing, an expression carrier pSilencer-siK-Ras was constructed, and the EC9706 cell linewas transfected using a liposome technique. Six groups were established: Control, siRNA NC (transfected withempty vector pSilencer2.1); Ras siRNA (transfected with pSilencer-siK-Ras2); Paclitaxel; Paclitaxel + siRNANC; and Ras siRNA + Paclitaxel. After the treatment, RT-PCR, Western blotting, MTT assay, flow cytometryand the Transwell technique were used to assess expression of K-Ras mRNA and protein in EC9706 cells, aswell as cell growth, proliferation, apoptosis and invasiveness. The effect of Paclitaxel chemotherapy was alsotested. pSilencer-siK-Ras2 effectively down-regulated expression of K-Ras mRNA and protein in EC9706 cells,growth being significantly inhibited. Flow cytometry indicated obvious apoptosis of cells in the experimentalgroup, with arrest in the G1 phase; cell migration ability was also reduced. After pSilencer-siK-Ras2 transfectionor the addition of Paclitaxel, EC9706 cells were suppressed to different extents; the suppressive effect wasstrengthened by combined treatment. The results suggested that RNAi-induced K-Ras gene silencing couldenhance chemotherapy sensitivity of esophageal cancer.