Effect And Mechanism Of PRMT2 On The Autophagy Of Breast Cancer MCF-7 Cells

Objective:To investigate the effect of stable over expressed protein arginine methyl transferase 2(protein arginine methyltransferase 2 and prmt2) on autophagy of human breast cancer MCF-7 cell and its potential molecular mechanism.Methods:Establish stable over expressed PRMT2 MCF-7 cell line,PRMT2 was overexpressed after induced by Doxycycline;by using the transmission electron microscope to observe the effects of autophagy(autophagic vesicle) by PRMT2;to identify the expression of autophagy related proteins of PRMT2 stable over expressed MCF-7 cells by cyto-immunofluorescence;autophagy related proteins of MCF-7 cells with PRMT2 gene over expressed were examined by WB;the proteins were examined by WB,to further prove and analysis the effect of PRMT2 and the mechanism of PRMT2 on the autophagy of MCF-7 cell.Results:1.Transmission electron microscope observes the change of autophagy(autophagic vesicle) :the number of autophagosome decreased in stable over expressed PRMT2 MCF-7 cells and in a time-dependent.2.Cyto-immunofluorescence showed that PRMT2 over expressed MCF-7 decreasing the expression of LC3A/B.3.WB detected that stable over expressed PRMT2 in MCF-7 cells decrease the expression of LC3A/B and Beclin1 and in a time-dependent.4. The analysis of data of antibody array demonstrate PRMT2 inhibit the phosphorylation of mTOR in MCF-7 cell, WB shows an decrease of expression of phosphorylation of AMPK and ULK1.Conclusions:1.PRMT2 inhibit autophgagy of human breast cancer MCF-7 cell in vitro and in a time-dependent.2.PRMT2 might down-regulates the AMPK/ULK1 signaling pathway to inhibit autophagy of human breast cancer MCF-7 cells.