MIAO Jian, MA Tao, LI Nan, ZHANG Song-song, HUO Qiang, WU Cheng-zhu. Effect of magnolol glucoside on the proliferation, invasion and migration of human breast cancer cells[J]. Journal of Bengbu Medical University, 2018, 43(5): 567-572. DOI: 10.13898/j.cnki.issn.1000-2200.2018.05.002
    Citation: MIAO Jian, MA Tao, LI Nan, ZHANG Song-song, HUO Qiang, WU Cheng-zhu. Effect of magnolol glucoside on the proliferation, invasion and migration of human breast cancer cells[J]. Journal of Bengbu Medical University, 2018, 43(5): 567-572. DOI: 10.13898/j.cnki.issn.1000-2200.2018.05.002

    Effect of magnolol glucoside on the proliferation, invasion and migration of human breast cancer cells

    • Objective: To investigate the effects of magnolol-2-O-β-D-glucopyranoside(Mag-glu) on the proliferation,invasion and migration of human breast cancer cells,and its possible mechanism.Methods: The effects of Mag-glu on the proliferation of MCF-7 and MDA-MB-231 cells were detected using MTT assay.The effects of Mag-glu on the migration and invasion ability of human breast cancer cells were analyzed using the wound healing assay and transwell assay,respectively.The effects of Mag-glu on the expression levels of hypoxia-inducible factor 1α(HIF-1α),matrix metalloproteinase-9(MMP-9) and cyclooxygenase-2(COX-2) were detected using Western blotting.Results: Mag-glu could inhibit the proliferation of MCF-7 and MDA-MB-231 cells in a concentration-and time-dependent manner.The migration ability of MDA-MB-231 cells decreased significantly after 24 h of treatment with Mag-glu(P<0.01).Transwell assay results showed that cell migration and invasion abilities significantly decreased after 24 h and 48 h of treatment with different concentrations of Mag-glu.The expression levels of HIF-1α,MMP-9 and COX-2 down-regulated with the increasing of the concentration of Mag-glu.Conclusions: Mag-glu can inhibit the proliferation,invasion and migration of human breast cancer cells in vitro,the mechanism of which may be inhibiting the HIF-1α signaling pathway to lead to the down-regulated expression of COX-2 and MMP-9.
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