IADR Abstract Archives
Study the Inhibitory Effect on the Migration of Sulforaphane on Oral Cancer Cells
Objectives: Sulforaphane is a compound derived from cruciferous plants, like broccoli, cabbage and cauliflower etc. Recent studies have implicated that sulforaphane exerts antioxidative, anti-inflammatory, anti-angiogenesis and anticancer activities. However, the anticancer effects and related molecular mechanism of sulforaphane in human oral cancer cells have not been reported. Hence, we aim to clarify the molecular mechanism of sulforaphane in oral cancer.
Methods: In this study, we investigated the anti-metastasis effects of sulforaphane on both SCC-9 and SCC-14 oral cancer cells and examined the potential inhibitory mechanisms involved. In addition, to identify the molecular targets of sulforaphane, human proteinase array analysis was performed.
Results: Herein, we found that sulforaphane significantly inhibited the migratory and invasive abilities of both SCC-9 and SCC-14 oral cancer cells with 10 μM. Human proteinase array data showed that cathepsin S was reduced after sulforaphane treatment. In addition, significant down-regulation of metastatic ability can be observed in oral cancer cells treated with cathepsin S siRNA and inhibitor of cathepsin S (Z-FL-COCHO). Sulforaphane also exerted an inhibitory effect on phosphorylation of extracellular signal–regulated kinases (ERKs) and p38 MAPK subfamily.
Conclusions: Taken together, our results suggested that sulforaphane may have potential as antitumor agents in human oral cancer.
Methods: In this study, we investigated the anti-metastasis effects of sulforaphane on both SCC-9 and SCC-14 oral cancer cells and examined the potential inhibitory mechanisms involved. In addition, to identify the molecular targets of sulforaphane, human proteinase array analysis was performed.
Results: Herein, we found that sulforaphane significantly inhibited the migratory and invasive abilities of both SCC-9 and SCC-14 oral cancer cells with 10 μM. Human proteinase array data showed that cathepsin S was reduced after sulforaphane treatment. In addition, significant down-regulation of metastatic ability can be observed in oral cancer cells treated with cathepsin S siRNA and inhibitor of cathepsin S (Z-FL-COCHO). Sulforaphane also exerted an inhibitory effect on phosphorylation of extracellular signal–regulated kinases (ERKs) and p38 MAPK subfamily.
Conclusions: Taken together, our results suggested that sulforaphane may have potential as antitumor agents in human oral cancer.