アブストラクト（33巻2号：The Bulletin of Kanagawa Dental College）

The Bulletin of Kanagawa Dental College

English

Title　： Epidermal Growth Factor Mediates Down Regulation of BRAK / CXCL14 expression in Head and Neck Squamous Cell Carcinoma - Role of BRAK / CXCL 14 in Tumor Growth In Vivo -
Subtitle　： Selective Proceedings of 39th General Meeting of Kanagawa Odontological Society, 2004
Authors　： Shigeyuki Ozawa1), Yasumasa Kato2),3), Yojiro Maehata2), Eiro Kubota1),3), Ryu-Ichiro Hata2),3)
Authors（kana）　：
Organization　： 1)Department of Oral and Maxillofacial Surgery, Kanagawa Dental College, 2)Department of Biochemistry and Molecular Biology, Kanagawa Dental College, 3)Oral Health Science Research Center, Kanagawa Dental College
Journal　： The Bulletin of Kanagawa Dental College
Volume　： 33
Number　： 2
Page　： 112-114
Year/Month　： 2005 / 9
Article　： Report
Publisher　： Kanagawa Odontological Society
Abstract　： [ABSTRACT] BRAK / CXCL14, which is a CXC chemokine, known to induce B cell, monocyte, and dendritic cell infiltration and to inhibit angiogenesis. Recent studies have shown that BRAK expressed abundantly in normal tissues but absent or expressed only n a very small amount in certain carcinomas. In the present study, new down stream targets of epidermal growth factor receptor had been explored by cDNA microarray, and we identified BRAK as one of the genes down-regulated by EGF treatment of the human HSC-3 tongue sqamous cell carcinoma (SCC) cell line. To determine that inhibitory effect of EGF on BRAK expression is not restricted to HSC-3 cells, we tested 9 other kinds of squamous cell carcinoma cell lines. BRAK mRNA expression was found in 6 out of these 9 cell lines and this expression was inhibited by EGF treatment. On the other hand, in a non-BRAK-expressing cell line, KB, BRAK expression was restored by 5-azacytidine treatment, suggesting that BRAK gene expression in KB cells was inhibited by methylation of the gene. The tumor burden formed was smaller in stable BRAK-expressing vector transfected tumor cells than in mock transfectants. These results suggest that suppression of BRAK by EGF could be caused by gene methylation and that therapy using EGF receptor tyrosine kinase inhibitors may have clinical efficacy through, in part, restored immune response, i. e. through restoration of BRAK expression.
Practice　： Dentistry
Keywords　： BRAK, CXCL14, EGF, cDNA microarray, transfection, gene methylation