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pmid26617743
      Int+J+Clin+Exp+Pathol 2015 ; 8 (9 ): 10355-64
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  • Xanthatin, a novel potent inhibitor of VEGFR2 signaling, inhibits angiogenesis and tumor growth in breast cancer cells #MMPMID26617743
  • Yu Y ; Yu J ; Pei CG ; Li YY ; Tu P ; Gao GP ; Shao Y
  • Int J Clin Exp Pathol 2015[]; 8 (9 ): 10355-64 PMID26617743 show ga
  • Anti-angiogenesis targeting vascular endothelial growth factor receptor 2 (VEGFR2) has emerged as an important tool for cancer treatment. In this study, we described a novel VEGFR2 inhibitor, xanthatin, which inhibits tumor angiogenesis and growth. The biochemical profiles of xanthatin were investigated using kinase assay, migration assay, tube formation, Matrigel plug assay, western blot, immunofluorescence and human tumor xenograft model. Xanthatin significantly inhibited growth, migration and tube formation of human umbilical vascular endothelial cell as well as inhibited vascular endothelial growth factor (VEGF)-stimulated angiogenesis. In addition, it inhibited VEGF-induced phosphorylation of VEGFR2 and its downstream signaling regulator. Moreover, xanthatin directly inhibit proliferation of breast cancer cells MDA-MB-231. Oral administration of xanthatin could markedly inhibit human tumor xenograft growth and decreased microvessel densities (MVD) in tumor sections. Taken together, these preclinical evaluations suggest that xanthatin inhibits angiogenesis and may be a promising anticancer drug candidate.
  • |Angiogenesis Inhibitors/*pharmacology [MESH]
  • |Breast Neoplasms/*metabolism/pathology [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Movement/drug effects [MESH]
  • |Cell Proliferation/*drug effects [MESH]
  • |Female [MESH]
  • |Furans/*pharmacology [MESH]
  • |Humans [MESH]
  • |Neovascularization, Pathologic/*metabolism/pathology [MESH]
  • |Phosphorylation/drug effects [MESH]
  • |Signal Transduction/*drug effects [MESH]


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