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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 G2/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 iodide- (V+/PI-) cells, the cleavage of 116-kDa 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.

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