Effect Of PRMT2 On The Invasion And Migration Of MCF7 Cells And Its Mechanism

Objective: To investigate the effect of PRMT2 on invasion and migration of human breast cancer MCF-7 cell and its potential mechanism.Methods:1 To observe the morphological alternations of human breast cancer MCF-7 cell with over-expression of PRMT2, and by adopting transwell and scratch injury to observe the effect of PRMT2 on invasion and migration of MCF-7 cell. 2 By adopting western blot to detect the expression of EMT-related proteins of MCF-7 cell with PRMT2 gene over expressed and knocked down, and by adopting immunofluorescence to identify the expression and the translocation of E-cadherin of MCF-7. 3 By adopting antibody array to detect and select the cancer relevant signaling pathways with over-expression of PRMT2, by adopting western blot to demonstrate the mechanism of invasion of human breast cancer cell.Results: 1 Observation, statistical analysis of transwell and scratch injury data reveal: over-expression of PRMT2 contributes to an EMT-like morphological alterations, invasion, and migration in vitro, of MCF-7 cell. 2 Western blot detectations reveal that over-expression of PRMT2 in MCF-7 cell increase the expression of Slug, and suppress the expression of E-cadherin, reversely, knocking down of PRMT2 increase the expression of E-cadherin, while decrease the expression of Slug. The immunofluorescence pictures suggest an decreased expression of E-cadherin, yet no translocation has been oriented. 3 The analysis of data of antibody array demonstrate PRMT2 inhibit the phosphorylation of β-catenin in MCF-7 cell, western blot detectations reveal an decrease of expression of APC-Axin-GSK-3β complex, and an increase of translocation of β-catenin. Conclusion: 1. PRMT2 increase the invasion and migration of human breast cancer MCF-7 cell in vitro. 1. PRMT2 might activiate the Wnt signaling pathway through modulation of β-cataenin to contribute the invasion and migration of human breast cancer MCF-7 cell.