Elucidation of Epigenetics in Head and Neck Squamous Cell Carcinoma.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25293414
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Surgical dentistry
• Research Institution: Kanagawa Dental College
• Principal Investigator: Kubota Eiro 神奈川歯科大学, 歯学部, その他 (50170030)
• Co-Investigator(Kenkyū-buntansha): KONDO TADANORI 神奈川歯科大学, 歯学部, その他 (00587727) ; IKOMA TAKEHARU 神奈川歯科大学, 大学院歯学研究科, 助教 (10638290) ; OZAWA SHIGEYUKI 神奈川歯科大学, 大学院歯学研究科, 講師 (40434394) ; SUZUKI KENJI 神奈川歯科大学, 大学院歯学研究科, 講師 (80350536) ; MAEHATA YOUJIRO 神奈川歯科大学, 大学院歯学研究科, 講師 (80410009)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: CXCL14 / BRAK / 頭頚部癌 / メチル化

Outline of Final Research Achievements

We employed the CXCL14-expressing HSC-3 cells and the CXCL14-nonexpressing YCU-H891 cells as representatives of the two groups and compared their responses to cetuximab and their CXCL14 expression under various conditions. The growth of xenografted tumours initiated by HSC-3 cells, which expressed CXCL14 in vivo and in vitro, was suppressed by the injection of cetuximab into tumour-bearing mice, however neither the expression of the chemokine nor the cetuximab-dependent suppression of xenogarfted tumour growth were observed for YCU-H891 cells.
The inhibition of ERK MAP kinase signaling increased the levels of CXCL14 mRNA in HSC-3 cells, but not in YCU-H891 cells. We also found that the CXCL14 promoter region in YCU-H891 cells was hypermethylated, and that demethylation of the promoter by treatment with 5-aza-2’-deoxycytidine restored CXCL14 mRNA expression and in vivo cetuximab-mediated tumour-growth suppression.

Free Research Field

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