Induction of G2/M arrest and apoptosis by sulforaphane in human osteosarcoma U2-OS cells

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Sulforaphane is one of the most abundant isothiocyanates found in certain cruciferous vegetables, particularly broccoli. To date, sulforaphane has gained attention as a chemopreventive compound. The mechanism responsible for the anticancer effects of sulforaphane in osteosarcoma, however, is not clear. In this study, we demonstrate an anti-proliferative mechanism of sulforaphane in human osteosarcoma cells. The treatment of cells with sulforaphane resulted in a concentration- and time-dependent inhibition of growth and G(2)/M phase arrest of the cell cycle. This effect was associated with a decrease in protein expression of cyclin A and B1 and their activating partners, cyclin-dependent kinases (CDKs) 1 and 2, with concomitant up-regulation of p21, a CDK inhibitor. Sulforaphane treatment also resulted in apoptosis as evidenced by an increase in annexin V+/propidium (V+/PI-) cells, the cleavage of 116-k Da poly (ADP-ribose) polymerase (PARP) and ICAD and oligonucleosomal DNA fragmentation. Taken together, these findings indicate that the molecular mechanisms underlying sulforaphane-mediated growth inhibition in U2-OS cells may be the modulation of the cell cycle machinery and the induction of apoptosis.
Publisher
SPANDIDOS PUBL LTD
Issue Date
2011-09
Language
English
Article Type
Article
Citation

MOLECULAR MEDICINE REPORTS, v.4, no.5, pp.929 - 934

ISSN
1791-2997
DOI
10.3892/mmr.2011.520
URI
http://hdl.handle.net/10203/318809
Appears in Collection
MSE-Journal Papers(저널논문)
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