Sulforaphane enhances caspase-dependent apoptosis through inhibition of cyclooxygenase-2 expression in human oral squamous carcinoma cells and nude mouse xenograft model
- Authors
- Cho, Nam-Pyo; Han, Hye-Suk; Leem, Dae-Ho; Choi, In-Sun; Jung, Ji-Youn; Kim, Hyeong-Jin; Moon, Kyung-Suk; Choi, Kyeong-Hee; Soh, Yunjo; Kong, Gu; Cho, Sung-Dae; Choi, Seoung Hwan
- Issue Date
- Aug-2009
- Publisher
- ELSEVIER
- Keywords
- Human oral squamous cell carcinoma; Sulforaphane; Apoptosis; COX-2; bcl-2; Xenograft
- Citation
- ORAL ONCOLOGY, v.45, no.8, pp.654 - 660
- Indexed
- SCIE
SCOPUS
- Journal Title
- ORAL ONCOLOGY
- Volume
- 45
- Number
- 8
- Start Page
- 654
- End Page
- 660
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/176391
- DOI
- 10.1016/j.oraloncology.2008.07.003
- ISSN
- 1368-8375
- Abstract
- In this study, we found that oral squamous cell carcinomas (OSCCs) in Korean patients have a high level of COX-2 expression when compared with normal mucosa. Sulforaphane (SFN), rich in cruciferous vegetables, has been reported to display anti-cancer activity against many cancers. However, the effect and molecular mechanism of SFN in the proliferation of OSCC still remains unclear. To elucidate this mechanism, we investigated the anti-proliferative effect of SFN on KB and YD-10B cells and demonstrated that SFN significantly induced caspase-dependent apoptosis. Also, we observed that SFN inhibited COX-2 but not COX-1. In addition, bcl-2 protein, one of downstream targets of COX-2, was down-regulated by SFN. Furthermore, SFN also inhibited tumor growth in KB cell xenografts. These results show that SFN can act as a potent anti-oral cancer compound by inhibiting COX-2 activity.
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