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Allicin Inhibits Lymphangiogenesis in vitro and in vivo
Author(s) -
Wang Weicang
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.688.12
Subject(s) - allicin , lymphangiogenesis , in vivo , matrigel , lymphatic endothelium , chemistry , cancer research , endothelial stem cell , microbiology and biotechnology , in vitro , angiogenesis , lymphatic system , pharmacology , biology , biochemistry , immunology , metastasis , cancer , genetics
Allicin, the most abundant organosulfur compound in freshly crushed garlic, has been shown to inhibit tumor metastasis, however, the detailed mechanisms are largely unknown. Here we studied the effects of allicin on lymphangiogenesis, which is a critical step involved in tumor metastasis via generating new lymphatic vessels. Our results showed that allicin inhibited lymphangiogenesis in vitro and in vivo. In a Matrigel plug assay in mice, allicin inhibited the infiltration of podoplanin‐positive lymphatic endothelial cells induced by vascular endothelial growth factor C (VEGF‐C), suggesting its anti‐lymphangiogenic effects in vivo. In human microvascular lymphatic endothelial cells (HMVEC‐dLy), allicin showed its anti‐lymphangiogenic effects through inhibiting cell migration and tube formation. Allicin inhibited phosphorylation of VEGF receptor 2 (VEGFR2) and focal adhesion kinase (FAK) in a dose‐dependent manner, suggesting its regulatory effect on VEGF receptor pathway. Finally, S‐allylmercaptoglutathione (GSSA), a major metabolite of allicin, had no effect on lymphangiogenesis in HMVEC‐dLy cells. Together, our results demonstrate that allicin inhibited the lymphangiogenesis in vitro and in vivo, suggesting a novel mechanism for the health benefits of allicin.