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Journal of Cancer Prevention

Original Article

Cancer prevention research 2012; 17(4): 295-302

Published online December 30, 2012

© Korean Society of Cancer Prevention

Actin Cytoskeleton Architecture Regulates Sulforaphane-induced Differentiation in Human Chondrosarcoma, HTB-94 Cells

Won Kil Lee and Song Ja Kim


Sulforaphane (SFN) is an isothiocyanate, isolated from glucoraphanin in broccoli and other cruciferous vegetables. SFN is known to play roles such as anti-oxidant, anti-inflammation and anti-cancer effects. In this study, we observed that cell morphology was changed through disruption of actin cytoskeleton architecture by SFN treatment in chondrosarcoma cells, HTB-94. We previously demonstrated that polymerization of actin cytoskeletal architecture regulates differentiation in primary articular chondrocytes. So, we investigated the effects of SFN on differentiation in HTB-94. We founded that SFN increased the expression of type II collagen and SOX-9 as determined by western blot analysis. Also, SFN induced sulfated proteoglycan production as detected by Alcian blue staining. Based on this finding, we investigated whether SFN treatment changes the cell morphology signal to modulate SFN-induced differentiation. Cytochalasin D (CD) is a disruptor of actin cytoskeleton architecture and Jasplakinolide (Jas) is a stabilizing agent of cytoskeleton architecture. Treatment of CD and Jas regulate polymerization of cytoskeleton architecture in HTB-94 cells. CD treatment potentiated the SFN-induced expression of type II collagen. In contrast to the effects of CD, JAS treatment blocked SFN-induced type II collagen expression. Therefore, the above results suggest that SFN regulated differentiation via disruption of actin cytoskeleton architecture in human chondrosarcoma, HTB-94 cells. (Cancer Prev Res 17, 0-302, 2012)

Keywords: Chondrosarcoma, Sulforaphane, Differentiation, Cytoskeleton

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