Magnolol Suppresses Vascular Endothelial Growth Factor-Induced Angiogenesis by Inhibiting Ras-Dependent Mitogen-Activated Protein Kinase and Phosphatidylinositol 3-Kinase/Akt Signaling Pathways
作者： Ki Mo Kim , No Soo Kim , Jinhee Kim , Jong-Shik Park , Jin Mu Yi
DOI: 10.1080/01635581.2013.828082
关键词: Angiogenesis 、 PI3K/AKT/mTOR pathway 、 Cell biology 、 Chemistry 、 Vascular endothelial growth factor 、 Biphenyl compound 、 Protein kinase B 、 Magnolol 、 Proto-oncogene tyrosine-protein kinase Src 、 MAPK/ERK pathway 、 Molecular biology
摘要: Magnolol, a hydroxylated biphenyl compound isolated from Magnolia officinalis, has been reported to possess anticancer activity. Recent studies have also demonstrated that magnolol inhibits cell growth and induces the apoptosis of cancer cells. However, effects on vascular endothelial factor (VEGF)-induced angiogenesis in cells not studied. In present study, we used human umbilical vein (HUVECs) investigate antiangiogenic effect molecular mechanism magnolol. Magnolol inhibited VEGF-induced proliferation, chemotactic motility tube formation HUVECs vitro as well vessel sprouting aorta ex vivo. Furthermore, Ras activation subsequently suppressed extracellular signal-regulated kinase (ERK), phosphatidylinositol-3-kinase (PI3K)/Akt p38, but Src focal adhesion (FAK). Interestingly, knockdown by short interfering RNA produced inhibitor...
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