Effect Of HMGA1 Lowexpression On Invasiveness And Glycolytic Pathways Of T47D And MCF7 Cells

Objective To investigate the effects and possible mechanism of high-mobility group A1(HMGA1)on the invasion and glycolytic metabolism of breast cancer T47 D and MCF7 cells.MethodsT47D and MCF7 cells were cultured in vitro as the research object,the experiment was divided into three groups: T47 D and MCF7 cells without lentivirus infection were blank control group,LV-CON077 cell group was negative control group and LV-HMGA1-RNA cell group was HMGA1 low expression group.The follwing are the specific methods:1.Observing the effect of infection by immunofluorescence.Detect the expression of HMGA1 by Western Blot(P<0.01).2.Detecting the effect of low expression of HMGA1 on cell proliferation and clone formation by MTT and Clone formation Test(P<0.05).Exploring the effect of low expression of HMGA1 on cell invasion by Transwell experiment(P<0.01).3.Analyzing the expression of Epithelial-Mesenchymal Transition(EMT)related factors after low expression of HMGA1 by WB technique(P<0.05).4.To analyze the expression of glycolytic enzymes after low expression of HMGA1 by WB technique(P<0.05).Results1.Lentivirus infection in T47 D and MCF7 cells could be detected by Immunofluorescence.WB test showed that the expression of HMGA1 was decreased.2.The experiment of MTT and Clone formation indicated that the low expression of HMGA1 could highly inhibit the proliferation and clone formation of T47 D and MCF7 cells.Transwell experiment showed that the invasion ability of T47 D and MCF7 cells decreased after the low expression of HMGA1.3.WB test showed that the expression of E-Cadherian increased and N-Cadherian?Snail?Slug decreased in the low expression group of HMGA1.4.WB test showed that the expression of glycolytic key enzymes,such as LDHA in T47 D and MCF7 cells were increased,PFKFB2 and PDHK1 were decreased in T47 D and MCF7 cells,but Hexokinase-1did not change.Conclusion1.Low expression of HMGA1 may inhibit the proliferation ? invasion and EMT transformation of breast cancer T47 D and MCF7 cells by affecting the expression of key enzymes in glycolysis.