2019 Fiscal Year Final Research Report
Integrated analysis of oncogene candidates MYNN and p53 and elucidation of lung cancer development mechanism
Project/Area Number |
16K10460
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General surgery
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Research Institution | Okayama University |
Principal Investigator |
Ito Sachio 岡山大学, 医歯薬学総合研究科, 助教 (30335624)
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Co-Investigator(Kenkyū-buntansha) |
笹井 香織 岡山大学, 医歯薬学総合研究科, 助教 (50722162)
阪口 政清 岡山大学, 医歯薬学総合研究科, 教授 (70379840)
片山 博志 岡山大学, 医歯薬学総合研究科, 准教授 (90713975)
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Project Period (FY) |
2016-04-01 – 2020-03-31
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Keywords | MYNN / BTB/POZ / p53 / Lung cancer |
Outline of Final Research Achievements |
The novel oncogene Myoneurin (MYNN) belongs to the BTB / POZ-Zinc Finger protein family. MYNN has a high frequency of gene amplification in lung cancer, ovarian cancer, esophageal cancer, breast cancer, etc. Amplification of the MYNN-encoded chromosome 3q26 region has been confirmed in many cancers, and in recent years, the Cancer driver gene has been actively identified from this region. Since MYNN has strong transcription repressing ability, tumorigenicity, and p53 binding ability, it was considered that functional analysis of MYNN is very important for understanding carcinogenesis. In this study, we have presented new findings on the functional interaction between MYNN and p53.
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Free Research Field |
細胞生物学
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Academic Significance and Societal Importance of the Research Achievements |
本研究では、これまで機能未知であったがん遺伝子MYNNについての新しい知見を示した。MYNNとp53の発現バランスは細胞を通常状態に維持するために必要で、MYNNが過剰発現し発現バランスが崩れることでp53の機能を阻害し細胞が癌化する機能を獲得する可能性が示唆された。このことは肺癌発症のメカニズムを解明する上で有益な学術的意義を持ち、さらには癌の早期発見・治療応用・予後管理へと発展できるための社会的意義があると考える。
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