The Study Of EMT And It’s Mechanism In Pancreatic Cancer Cell Line PANC1 Through Knockdown Of MSX2

Objective: The purpose of this study was to investigate wether si MSX2 can promote MET in pancreatic cancer cell line PANC1, and the mechanism during this procedure.Methods: 1. The si RNA against MSX2 was transfected into PANC1 cells with Lipofectamine2000. The expression of MSX2 was detected by Realtime RT-PCR. 2. Compare the morphological changes between the si MSX2 and control group through microscope. 3. The Real-time RT-PCR and western-blot were used to detect the changes of E-cadherin and vimentin in gene and protein levels. 4. The expression of MET-relate gene snail、slug、twist、zeb1 was detected by RT-PCR in order to find the target gene of MSX2 influence of MET. 5. Cells migration and invasion capability in si MSX2 PANC1 was detected by Wound scratch assay and Tanswell assay, and the proliferation were detected by CCK-8 kit.Results: The cells in si MSX2 became cobblestone- like phenotype and get junctions compare to control group. MET-relate gene E-cadherin was upregulated in gene and protein levels, and vimentin was downregulated in si MSX2 panc1 which indicate the MET(P<0.05). The migration, invasion and proliferation was inhibited in si MSX2 cells compare to control groups. Transcription factor twist and snail was downregulated after interference of MSX2(P<0.05).Conclusion: Downregulation of MSX2 can reverse EMT, and induce MET in PANC1 cells. Farther more twist and snail may be target gene of MSX2 induce EMT in panc1 cel s. MSX2 gene may be used as an appropriate key point for molecular targeted therapy of pancreatic cancer.