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RNAi-induced K-Ras Gene Silencing Suppresses Growth of EC9706 Cells and Enhances Chemotherapy Sensitivity of Esophageal Cancer
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  • RNAi-induced K-Ras Gene Silencing Suppresses Growth of EC9706 Cells and Enhances Chemotherapy Sensitivity of Esophageal Cancer
  • RNAi-induced K-Ras Gene Silencing Suppresses Growth of EC9706 Cells and Enhances Chemotherapy Sensitivity of Esophageal Cancer
저자명
Wang. Xin-Jie,Zheng. Yu-Ling,Fan. Qing-Xia,Zhang. Xu-Dong
간행물명
Asian Pacific journal of cancer prevention : APJCP
권/호정보
2012년|13권 12호|pp.6517-6521 (5 pages)
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아시아태평양암예방학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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To analyze the growth, proliferation, apoptosis, invasiveness and chemotherapy sensitivity of EC9706 cells after K-Ras gene silencing, an expression carrier pSilencer-siK-Ras was constructed, and the EC9706 cell line was transfected using a liposome technique. Six groups were established: Control, siRNA NC (transfected with empty vector pSilencer2.1); Ras siRNA (transfected with pSilencer-siK-Ras2); Paclitaxel; Paclitaxel + siRNA NC; and Ras siRNA + Paclitaxel. After the treatment, RT-PCR, Western blotting, MTT assay, flow cytometry and the Transwell technique were used to assess expression of K-Ras mRNA and protein in EC9706 cells, as well as cell growth, proliferation, apoptosis and invasiveness. The effect of Paclitaxel chemotherapy was also tested. 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 experimental group, with arrest in the G1 phase; cell migration ability was also reduced. After pSilencer-siK-Ras2 transfection or the addition of Paclitaxel, EC9706 cells were suppressed to different extents; the suppressive effect was strengthened by combined treatment. The results suggested that RNAi-induced K-Ras gene silencing could enhance chemotherapy sensitivity of esophageal cancer.