Abstract Title:

Sulforaphane Increases Cyclin-Dependent Kinase Inhibitor, p21 Protein in Human Oral Carcinoma Cells and Nude Mouse Animal Model to Induce G(2)/M Cell Cycle Arrest.

Abstract Source:

J Clin Biochem Nutr. 2010 Jan;46(1):60-7. Epub 2009 Dec 29. PMID: 20104266

Abstract Author(s):

Jun-Hee Kim, Ki Han Kwon, Ji-Youn Jung, Hye-Suk Han, Jung Hyun Shim, Sejun Oh, Kyeong-Hee Choi, Eun-Sun Choi, Ji-Ae Shin, Dae-Ho Leem, Yunjo Soh, Nam-Pyo Cho, Sung-Dae Cho

Article Affiliation:

Department of Oral Pathology, School of Dentistry and Institute of Oral Bioscience, Brain Korea 21 project, Chonbuk National University, Jeonju, 561-756, Republic of Korea.


Previously, our group reported that sulforaphane (SFN), a naturally occurring chemopreventive agent from cruciferous vegetables, effectively inhibits the proliferation of KB and YD-10B human oral squamous carcinoma cells by causing apoptosis. In this study, treatment of 20 and 40 microM of SFN for 12 h caused a cell cycle arrest in the G(2)/M phase. Cell cycle arrest induced by SFN was associated with a significant increase in the p21 protein level and a decrease in cyclin B expression, but there was no change in the cyclin A protein level. In addition, SFN increased the p21 promoter activity significantly. Furthermore, SFN induced p21 protein expression in a nude mouse xenograft model suggesting that SFN is a potent inducer of the p21 protein in human oral squamous carcinoma cells. These findings show that SFN is a promising candidate for molecular-targeting chemotherapy against human oral squamous cell carcinoma.

Study Type : Transgenic Animal Study

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