Sulforaphane inhibits human MCF-7 mammary cancer cell mitotic
progression and tubulin polymerization
Sulforaphane (SUL), an isothiocyanate derived from hydrolysis
of glucoraphanin in broccoli and other cruciferous vegetables,
was shown to induce phase II detoxification enzymes, inhibit
chemically induced mammary tumors in rodents, and more recently,
to induce cell cycle arrest and apoptosis in colon cancer
cells. In the present study, we demonstrate that SUL also
acts to inhibit proliferation of MCF-7 adenocarcinoma cells
from the human breast. Treatment of synchronized MCF-7 cells
with 15 micromol/L SUL resulted in significant (P < 0.05)
G(2)/M cell cycle arrest (167% of control) and elevated cyclin
B1 protein (175% of control) within 24 h. Moreover, 15 micromol/L
SUL significantly (P < 0.05) induced phosphorylation of
histone H1 (167% of control), blocked cells in early mitosis
( approximately 10-fold increase over control), and disrupted
polymerization of mitotic microtubules in vivo. Subsequent
exposure of purified bovine brain tubulin to relatively high
doses of SUL significantly (P < 0.05) inhibited both tubulin
polymerization rate (51% of control) and total tubulin polymerization
(78% of control) in vitro. Additionally, polymerization of
purified tubulin exposed to isothiocyanate-containing analogs
of SUL was similarly inhibited. Taken together, these findings
indicate that SUL has mammary cancer suppressive actions involving
mitotic cell cycle arrest and suggest a mechanism linked to
the disruption of normal tubulin polymerization and/or more
subtle effects on microtubule dynamics. Jackson SJ, Singletary
KW. J Nutr. 2004 Sep;134(9):2229-36.
The preceding abstract was obtained from the Medline service maintained by the
National Institutes of Health.
For educational purposes only. Consult your physician for
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*These statements have not been evaluated by the Food &
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