| Project/Area Number |
15K10817
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
MAKOTO KUROSE 札幌医科大学, 医学部, 講師 (60404696)
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| Co-Investigator(Kenkyū-buntansha) |
高野 賢一 札幌医科大学, 医学部, 准教授 (70404689)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | Head and neck cancer / squamous cell carcinomas / JAM-A / p63/GATA-3 / HDAC / malignancy / 頭頸部扁平上皮癌 / 悪性化 / シグナル伝達経路 / HDAC阻害剤 / NF-ｋBシグナル |
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| Outline of Final Research Achievements |
In the present study, we investigated the possibility about auxiliary diagnosis and targeted therapy of squamous cell carcinomas in head and neck cancer by tight junction related molecule JAM-A. We found high expression of JAM-A at the protein and mRNA levels in head and neck squamous cell carcinoma (HNSCC) tissue. Soluble JAM-A in serum of HNSCC patients was high level compared to the normal. Overexpression of JAM-A in HNSCC cell line Detroit562 was in part regulated via p63/GATA-3. We used inhibitors of histone deacetylase (HDAC). By using HNSCC cell line Detroit562, treatment with a panHDAC inhibitor tricostatin A (TSA) or specific inhibitors of HDAC1 and HDAC6 prevented the invasion, migration and proliferation of cancer cells in vitro. Furthermore, they also inhibited expression of p63 and JAM-A in Detroit562 cells. Taken together, inhibitors of HDAC are available in possible about auxiliary diagnosis and molecular targeted therapy for HNSCC via p63/JAM-A.
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