Lipid Analogues BML-111 Inhibited The Proliferation,EMT And Migration Of Breast Cancer Cells MCF-7 By Down-regulating 5-LOX

Objective:Breast cancer is one of the common cancers that endanger the life and health of women.At present,breast cancer has gradually become the leading cause of life and threatening women's health in our economically developed areas.Lipoxygenase(LOX)plays an important role in the development of various tumors.We speculate that lipid analogues BML-111 may inhibit LOX to prevent the development of breast cancer.Therefore,In this experiment,we use BML-111 to treat MCF-7,observing the changes of proliferation,epithelial mesenchymal transition(EMT)and migration,and exploring its mechanism preliminary,which provide experimental basis for the clinical manifestations of breast cancer.Methods:1 MTT assay was used to detect the effects of different concentrations and times of BML-111 on the survival rate of MCF-7.2 Using inverted microscope to observe the EMT changes in different treated cells.3 Wound Healing assay and transwell experiment were used to detect the effects of BML-111 on the migration ability in CoCL2-induced MCF-7 cells.4 Using Western blotting(WB)to detect the effects of BML-111 on the expression of 5-LOX,12-LOX and 15-LOX,E-Cadherin,Vimentin,MMP-2 and MMP-9 in CoCL2-induced MCF-7 cells.Res?lts:1 MTT results: BML-111 has concentration and time dependence on MCF-7 cells viability.2 EMT changes: The effects of BML-111 on CoCL2-induced MCT-7 cells were as follows: The EMT ability of CoCL2 group was higher than that in control group(P < 0.05);CoCL2+BML-111 group was inhibited compared with CoCL2 group(P < 0.05);CoCL2 + BML-111 + Boc-2 group was increased compared with CoCL2 + BML-111 group(P < 0.05).3 Wound Healing assay results: The migration ability of BML-111 on CoCL2-induced MCF-7 cells were as follows:Compared with the control group,cells migration ability of CoCL2 group significantly increased(P < 0.01);Compared with the CoCL2 group,cells migration ability of CoCL2 + BML-111 group significantly weakened(P < 0.01);Compared with CoCL2 + BML-111 group,cells migration ability of CoCL2 + BML-111+BOC-2 group increased(P < 0.05).4 Transwell experiment results: The migration ability of BML-111 on CoCL2-induced MCF-7 cells were as follows: Compared with the control group,cells migration ability of CoCL2 group increased(P < 0.05);Compared with the CoCL2 group,cells migration ability of CoCL2 + BML-111 group weakened(P < 0.05);Compared with CoCL2 + BML-111 group,cells migration ability of CoCL2 + BML-111+BOC-2 group increased(P < 0.05).5 Western blotting results: The expression of Vimentin,MMP-2,MMP-9 and 5-LOX of CoCL2 group were higher than those in control group,and the expression of E-Cadherin was lower(P <0.05);Compared with CoCL2 group,the expression of Vimentin,MMP-2,MMP-9 and 5-LOX of CoCL2 + BML-111 group were lower,and the expression of E-Cadherin was higher(P < 0.05);Compared with CoCL2 + BML-111 group,the expression of Vimentin,MMP-2,MMP-9 and 5-LOX of CoCL2 + BML-111 + Boc-2 group were higher,and the expression of E-Cadherin was lower(P < 0.05).There was no significant difference between 12-LOX and 15-LOX in each group(P > 0.05).Conclusion:1 BML-111 can inhibit the proliferation of MCF-7 cells.2 BML-111 can inhibit the EMT and migration ability of CoCL2-induced MCF-7 cells.3 BML-111 may inhibit the EMT and migration ability of CoCL2-induced MCF-7 cells by down-regulating 5-LOX.