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Curcumin induces endothelial mitotic arrest and disrupts tubulin polymerization
Author(s) -
Jackson Steven J. T.,
Venema Richard C.
Publication year - 2007
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.21.5.a361
Subject(s) - curcumin , angiogenesis , microbiology and biotechnology , mitosis , microtubule , microtubule polymerization , tubulin , endothelial stem cell , cell cycle checkpoint , colchicine , chemistry , cell cycle , biology , in vitro , biochemistry , cell , cancer research , genetics
Curcumin (CMN), a component of turmeric spice that imparts flavor and color to curry, is a known anti‐inflammatory and angiogenesis‐suppressing bioactive agent. Here, we provide the first evidence that CMN inhibits endothelial cell proliferation via a mechanism involving microtubule depolymerization and mitotic cell cycle arrest. Exposure of bovine aortic endothelial (BAE) cells to 15 μM CMN resulted in significant (P<0.05) inhibition of DNA synthesis (26% of control) and G 2 /M accumulation (~10‐fold increase over control) within 24 h. Moreover, this same CMN treatment was found to trigger early M‐phase cell cycle arrest together with disruption of endothelial mitotic (and cytoplasmic) microtubules. Subsequent exposure of purified bovine tubulin proteins to 15 μM CMN resulted in significant (P<0.05) inhibition of tubulin polymerization rate in vitro . Taken together, these findings indicate that CMN impedes endothelial M‐phase progression and suggest a mechanism of angiogenesis suppression facilitated by disruption of mitotic microtubule polymerization and/or dynamics. (Supported by AICR and NIH)