| Project/Area Number |
17K11309
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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 |
Obstetrics and gynecology
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
KUKIMOTO IWAO 国立感染症研究所, 病原体ゲノム解析研究センター, 室長 (70291127)
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| Project Period (FY) |
2017-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | ヒトパピローマウイルス / 子宮頸がん / TEAD4 / Rb / HPV / E7 / RNA-seq / 子宮頸癌 / パピローマウイルス / APOBEC / 癌 / 感染症 / ウイルス |
|---|
| Outline of Final Research Achievements |
The human papillomavirus oncoprotein E7 is known to induce APOBEC3B gene expression, but the molecular mechanism is not clear. In this study, we show that E7 induces expression of the cellular transcription factor TEAD4 via binding to and degradation of Rb. TEAD4 is involved in APOBEC3B gene expression, suggesting that E7 induces APOBEC3B via TEAD4. E7s, encoded by three HPV16 variants (A1, A4, and A5) showing different risks of cervical cancer progression, were also found to alter expression patterns of different cellular genes.
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| Academic Significance and Societal Importance of the Research Achievements |
ヒトパピローマウイルス（HPV）の持続感染は子宮頸癌の原因であることから、HPV感染による子宮頸癌の発症メカニズムを解明することは、子宮頸癌の新たな治療・予防法の開発に結びつくと考えられる。本研究で、HPV癌タンパク質E7が細胞癌化を引き起こす分子機構の一端が明らかになり、HPV発癌機構の理解が進むことが期待される。
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