Sulforaphane enhances caspase-dependent apoptosis through inhibition of cyclooxygenase-2 expression in human oral squamous carcinoma cells and nude mouse xenograft model

Oral Oncol. 2009 Aug;45(8):654-60. doi: 10.1016/j.oraloncology.2008.07.003. Epub 2008 Sep 19.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anticarcinogenic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Carcinoma, Squamous Cell / enzymology*
  • Carcinoma, Squamous Cell / pathology
  • Caspases / physiology
  • Cyclooxygenase 2 Inhibitors / pharmacology*
  • Disease Models, Animal
  • Humans
  • Isothiocyanates
  • Mice
  • Mice, Nude
  • Mouth Neoplasms / enzymology*
  • Mouth Neoplasms / pathology
  • Republic of Korea
  • Sulfoxides
  • Thiocyanates / pharmacology*

Substances

  • Anticarcinogenic Agents
  • Cyclooxygenase 2 Inhibitors
  • Isothiocyanates
  • Sulfoxides
  • Thiocyanates
  • Caspases
  • sulforaphane