2016 Fiscal Year Final Research Report
A global study for HPV-cell infection mechanism
| Project/Area Number |
26462531
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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 | Yokohama City University |
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Principal Investigator |
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| Research Collaborator |
YAMASHITA Akio
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | HPV |
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| Outline of Final Research Achievements |
In this study, (1) we successfully obtained high titer of HPV virus-like particles using combination of optimal code usage and high expression cells. Using this HPV virus-like particles, we found that BP-1 may be a receptor of HPV, because the infection of HPV to cells was 35% decreased when the BP-1 was down-regulated. (2) E6 and E7 are major oncogenes of HPV. We newly identified an apoptosis relative protein named p55 bound to both E6 and E7 and their co-localization was confirmed. Overexpression of p55 increased sensitivity of cellular apoptosis, while suppression of p55 decreased the apoptosis. E6 degraded P55 by ubiquitination pathway. Therefore p55 plays an important role in E6-relative cervical cancer and p55 is a potent target for prophylaxis and therapy of cervical cancer.
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| Free Research Field |
ウイルス学
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