| Project/Area Number |
26860212
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KOMATSU Masato 徳島大学, 疾患プロテオゲノム研究センター, 助教 (50531753)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | TNBC / 核内PAG1 / PARP1 / トリプルネガティブ乳癌 / プロテアソーム構成因子 |
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| Outline of Final Research Achievements |
Triple negative breast cancers (TNBC) is one of the most aggressive subtype of breast cancers, and little is known about tumor aggressiveness. Based on the evidence through gene expression and immunohistochemical analyses that prognosis of TNBC patients with higher nuclear-PAG1 expression was worse than that with lower nuclear-PAG1 expression, we focused on the role of nuclear-PAG1 on the aggressiveness of TNBC. Then, we revealed that PARP1 might interact with nuclear-PAG1 through high-throughput proteomics analyses, 2DICAL. PARP1 is considered to be involved in DNA repair, and PARP inhibitors are currently approved to clinical setting for treatment of breast cancers including TNBC and ovarian cancers. Therefore, the interaction of nuclear-PAG1 and PARP1 might lead to alteration of the sensitivity of PAPR1 inhibitors in breast cancer cells.
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