Inhibiting K-ras Signaling Reserves the Epithelial-Mesenchymal Transition of Pancreatic Cancer Cells and its Mechanisms

Background/Aims: To investigate the effects of K-ras siRNA on pancreatic cancer cells and the expression levels of GLI1, E-cadherin and vimentin in pancreatic cancer cells transfected with K-ras siRNA. Methodology: Pancreatic cancer cells PANC-1 were transfected with K-ras siRNA. Growth inhibition ratio of the cells were measured by MTT assay, apoptosis was detected by flow cytometery, expression level of GLI1, E-cadherin and vimentin were detected by Western blot. Results: The expression of K-ras protein was efficiently inhibited by K-ras siRNA in PANC-1 cells. The growth inhibition rates of the cells were significantly different to the control groups. Apoptosis rates were significantly different with that of control group. The expression of GLI1 was significantly down-regulated, E-cadherin was up-regulated, while vimentin was also down-regulated in K-ras siRNA transfected cells compared with that of control groups. Conclusions: Inhibiting K-ras signaling by K-ras siRNA can inhibit proliferation and induce apoptosis of pancreatic cancer cells, down-regulate GLI1's and vimentin's expression, and up-regulate E-cadherin's expression. Inhibiting K-ras signaling by K-ras siRNA may reduce epithelial to mesenchymal transition of pancreatic cancer cell PANC-1.