The Effect And Mechanism Of MiR-181b/ZEB2 Feedback Pathway On The EMT In Pancreatic Cancer Cell

Background:Pancreatic cancer is a highly malignant tumor. It is not sensitive to radiotherapy and chemotherapy. Its 5% year survival rate is less than 5% [1]. Studies have found that in pancreatic cancer cells undergoing EMT process and E-cadherin was decreased, the expression of Vimentin increased, so that pancreatic cancer metastasis, and leads to poor prognosis [2,3].However, the current research on pancreatic cancer EMT upstream regulatory mechanism is not sufficient. EMT inhibitory regulation factor is particularly important,inhibiting the EMT of miRNAs in pancreatic cancer may be a diagnostic marker and therapeutic target.Purpose: The effect of miR-181b/ZEB2 feedback pathway on pancreatic cancer cell line SW1990 was detected.Method:1.The effect of MTT and flow cytometry on the proliferation of SW1990 cell line was detected by miR-181 b. 2. The expression of miR-181 b, Virnentin, ZEB2 and E-cadherln was measured by q-PCR and Western blotting in SW1990 cell line.3.The relationship between ZEB2 and miR-181 b promoter in SW1990 was measuredby ChIP-PCR.4.The effect of ZEB2 on the expression of miR-181 b was detected by dual luciferase reporter gene assay.Results: 1.miR-181 b promotes apoptosis of SW1990 cell line and inhibits its growth.2. After miR-181b-mimic transfection, the expression level of E-cadherln was significantly increased, and the expression level of Virnentin and ZEB2 were significantly decreased.3.ZEB2 and miR-181 b promoter was combined in SW1990 cell line.4. Dual luciferase reporter gene assay confirmed ZEB2 to hijack or inhibit the true transcription factor of miR-181 b.Conclusion: miR-181b/ZEB2 negative feedback pathway affect the proliferation andapoptosis of pancreatic cancer cells by regulating EMT.