| Project/Area Number |
15591837
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | ST.Marianna University School of Medicine |
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Principal Investigator |
TSUTSUMI Kouichiro St.Marianna University School of Medicine, Otolaryngology, lecturer, 医学部, 講師 (40217344)
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| Project Period (FY) |
2003 – 2005
|
| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2005: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | HPV16E7 / head and neck epithelial cells / p53 / 頭頸部上皮細胞 |
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| Research Abstract |
The tumor suppressor protein p53 has a short half-life in normal cells, and is stabilized upon DNA damage. Stabilization of p53 is an important component of the cellular response to oncogenic insults that can culminate in cellular growth arrest or apoptosis. The purpose of this study was to examine the effects of human papillomavirus type 16 E7 (16E7)-expression to p53 function in cultured human head and neck epithelial cells (HLECs). The p53 steady state levels were consistently two to four times higher in 16E7-expressing HLECs (16E7-HLECs) than in control normal HLECs (nHLECs) and the half-life of p53 was extended in 16E7-HLECs, suggesting that 16E7 can interfere with the normal turnover of p53. Expression profiling studies using cDNA arrays and immunoblot analyses of known p53 target genes suggest that p53 remains transcriptionally inert in 16E7-HLECs. Nevertheless,16E7-HLECs were more sensitive to Fas-mediated apoptosis (this apoptosis is reported to be p53 dependent) compared to nHLECs. Taken together, we could not determine whether the stabilized p53 is functionally active in 16E7-HLECs.
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