Fraxetin Inhibits MCF-7 Cell Proliferation and Migration through Inhibiting EGFR and Its Downstream AKT Signaling Pathway

epidermal growth factor receptor( EGFR) is an intersection of various of signaling pathways in cells,its signaling pathway is closely related with occurrence,development,metastasis and invasion of breast cancer,it has become one of new targets of breast cancer treatment. However,its anti-breast cancer mechanisms and relationship with EGFR signaling pathway were poorly studied. Our research indicated that,the anti-breast cancer activity of fraxetin mainly is to inhibit EGFR and its downstream AKT signaling pathway,fraxetin could promote the proliferation of T,B lymphocyte and improve the phagocytosis of macrophage in vitro,indicating that fraxetin could promote immune function in mice.Western blotting results indicated that fraxetin could inhibit the expression and activation of EGFR and AKT. Wound healing assay result showed that fraxetin could inhibit cell migration. In addition,fraxetin could significantly improve the immune function and the phagocytosis of macrophage, increase the proliferation of T,B lymphocyte and improve the killing activity of NK cells. The results suggested that the anti-breast cancer effects of fraxetin were inhibited cell migration,promoted the proliferation of T,Blymphocyte and improved the phagocytosis of macrophage and killing activity of NK cells through the EGFR and AKT signaling pathway.