| Project/Area Number |
21390543
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Kanagawa Dental College |
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Principal Investigator |
KUBOTA Eiro 神奈川歯科大学, 歯学部, 教授 (50170030)
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| Co-Investigator(Kenkyū-buntansha) |
MAEHATA Yojiro 神奈川歯科大学, 歯学部, 講師 (80410009)
SUZUKI Kenji 神奈川歯科大学, 歯学部, 歯学部 (80350536)
OZAWA Shigeyuki 神奈川歯科大学, 歯学部, 助教 (40434394)
KONDO Tadanori 神奈川歯科大学, 附属病院, 医員 (00587727)
KATO Yasumasa 神奈川歯科大学, 歯学部, 准教授 (50214408)
ITO Shin 神奈川歯科大学, 歯学部, 特別研究員 (00460139)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥18,200,000 (Direct Cost: ¥14,000,000、Indirect Cost: ¥4,200,000)
Fiscal Year 2011: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2009: ¥10,140,000 (Direct Cost: ¥7,800,000、Indirect Cost: ¥2,340,000)
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| Keywords | ケモカイン / BRAK / メチル化 / EGFR阻害剤 / 頭頸部扁平上皮癌 / CXCL14 / EGFR / SCC / Gefitinib / DAC / microarray / transcription |
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| Research Abstract |
BRAK/CXCL14 is a chemokine that is expressed in normal tissues, and is important for maintaining homeostasis. BRAK has many functions such as inhibition of angiogenesis and chemotaxis of monocytes as well as macrophaghes. BRAK is absent from or expressed at very low levels in head and neck squamous cell carcinoma(HNSCC), and this is closely correlated with tumorigenesis and progression of HNSCC. Forced expression of BRAK chemokine by the gene transfection into HNSCC or BRAK transgenic mice reduced the tumorigenicity of the cells in xenografts, and BRAK was considered to be a target molecule for the cancer treatment. In the present study, we elucidated that low expression of BRAK in HNSCC was due to mutation of BRAK promotor region by methylation. The low expression level of BRAK in HNSCC is restored by treatment of the cells with anti-methylation drug. HNSCC overexpressed BRAK by EGF receptor antagonist(gefitinib) and anti-methylation drug gave rise to susceptible to tumor regression. The anti-tumor effect using gefitinib and anti-cancer drugs is thus feasible for combination chemotherapy in HNSCC.
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