| Project/Area Number |
24650650
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Clinical oncology
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| Research Institution | 愛知県がんセンター(研究所) |
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Principal Investigator |
SEKIDO Yoshitaka 愛知県がんセンター(研究所), 分子腫瘍学部, 副所長 兼 部長 (00311712)
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| Co-Investigator(Kenkyū-buntansha) |
近藤 英作 愛知県がんセンター(研究所), 腫瘍病理学部, 部長 (30252951)
藤井 万紀子 愛知県がんセンター(研究所), 分子腫瘍学部, 主任研究員 (70406031)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 分子標的治療 / 悪性中皮腫 / ペプチド創薬 / 癌 / シグナル伝達系 / 転写因子 / トランスレーショナルリサーチ / シグナル伝達 |
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| Research Abstract |
Malignant mesothelioma (MM) is a very aggressive tumor and, currently, there are no effective chemotherapeutic drugs or molecular-target reagents against this fatal disease. In this project, we performed experiments to develop a new therapeutic modality against MM. Since MM shows frequent inactivation of p16INK4a tumor suppressor gene, we employed a functional peptide which is permeable through the cell membrane and restores p16 function. We found that this peptide induced apoptosis of MM cells very effectively and specifically, which seemed promising to be a new therapeutic tool. Furthermore, we also analyzed YAP oncogene product, which is constitutively activated and leads to more malignant phenotypes of MM cells. We clarified which members of TEAD family transcription factors, YAP binding partners, were important in deregulated MM cell proliferation. These findings were very indicative to develop a new strategy to regulate YAP protein as a therapeutic modality of MM.
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