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Decursin and decursinol inhibit VEGF-induced angiogenesis by blocking the activation of extracellular signal-regulated kinase and c-Jun N-terminal kinase

Title
Decursin and decursinol inhibit VEGF-induced angiogenesis by blocking the activation of extracellular signal-regulated kinase and c-Jun N-terminal kinase
Authors
Son S.H.Kim M.-J.Chung W.-Y.Son J.-A.Kim Y.S.Kim Y.-C.Kang S.S.Lee S.-K.Park K.-K.
Ewha Authors
이상국
Issue Date
2009
Journal Title
Cancer Letters
ISSN
0304-3835JCR Link
Citation
vol. 280, no. 1, pp. 86 - 92
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
The root of Angelica gigas Nakai contains two major coumarins, which have been previously identified as decursin and decursinol. Decursin has been demonstrated to exhibit potent anti-cancer activity both in vitro and in vivo. In this study, we found that decursin and decursinol at non-cytotoxic doses inhibited the VEGF-induced proliferation, migration, and capillary-tube formation of HUVECs. Moreover, decursin and decursinol suppressed microvessel formation on chorioallantoic membranes in fertilized eggs and into mouse Matrigel plugs. The oral administration of decursin and decursinol also reduced VEGF-induced angiogenesis in Matrigel. Furthermore, decursin and decursinol reduced the phosphorylation of ERK and JNK, but not p38 MAPK, in VEGF-stimulated HUVECs. Taken together, our results reveal that decursin and decursinol inhibit VEGF-induced angiogenesis by reducing the activation of ERK and JNK in HUVECs, and possess potent in vivo anti-angiogenic activity, coupled with the advantage of oral dosing. Thus, these compounds may have the potential for the treatment of cancers dependent on VEGF-induced vascularization. © 2009 Elsevier Ireland Ltd. All rights reserved.
DOI
10.1016/j.canlet.2009.02.012
Appears in Collections:
약학대학 > 약학과 > Journal papers
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