EFFECT OF THE NANOG GENE ON PROLIFERATION AND APOPTOSIS IN THE PANCREATIC CANCER CELL LINE PANC-1

Objective: To investigate the effect of the Nanog gene on proliferation and apoptosis in the pancreatic cancer cell line PANC-1 and explore its possible mechanism. Methods: The pancreatic cancer cell line PANC-1 was selected and transfected with the Nanog gene to over-express this gene as the over-expression group. Meanwhile, the blank control group (without any treatment) and negative control group (transfected with empty plasmid) were set up. The expression level of Nanog mRNA in each group of cells was detected using qPCR. The effects of Nanog gene on cell proliferation and apoptosis were measured by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and Hoechst 33258, respectively. Western-blot analysis was used to determine the expression of Bcl-2, Bax and Caspase3 proteins in the cells of each group. Then, the effect of Nanog on the JAK2/STAT3 signalling pathway was further verified. Results: The expression level of Nanog mRNA in the over-expression group was significantly higher than that in the blank control group and the negative control group (P<0.01). Moreover, the proliferation level of the cells in the over-expression group was obviously higher than in the blank control and negative control groups (P<0.01). The results of Hoechst 33258 staining showed that the level of apoptosis in the over-expression group was remarkably lower than in the blank control and negative control groups (P < 0.01). The expression level of Bcl-2/Bax, p-JAK2 and p-STAT3 in the over-expression group was significantly higher than in the blank control and negative control groups (P<0.01), and the Caspase3 expression level in the over-expression group was markedly lower than in the blank control and negative control groups (P<0.01). Conclusion: Nanog can promote the proliferation of the pancreatic cancer cell line PANC-1 and decrease apoptosis. The mechanism for this may be related to activation of the JAK2/STAT3 signalling pathway.