| Project/Area Number |
14571920
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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 |
Surgical dentistry
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| Research Institution | Kanagawa Dental College |
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Principal Investigator |
SASAKURA Yuuichi Kanagawa Dental College, Dentistry, Associate Professor, 歯学部, 助教授 (80121002)
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| Co-Investigator(Kenkyū-buntansha) |
MIYOSHI Yoshiko Kanagawa Dental College, Dentistry, Assistant Professor, 歯学部, 講師 (70288075)
LEE Ushyaku Kanagawa Dental College, Dentistry, Instructor, 歯学部, 助手 (90288085)
OHMI Yasushi Kanagawa Dental College, Dentistry, Instructor, 歯学部, 助手 (10318892)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | telomerase activity / hTERT / p53 gene / head and neck squamous cell carcinoma |
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| Research Abstract |
It is well known that telomerase activity (TA) is detected in a majority of malignant human tumors but not in normal somatic cells except for few kinds of cell lineages. It has also been reported that telomere is located on the end of eukaryotic chromosome, and its sufficient length is essential for chromosome stabilization. In addition, there are reports describing that the reactivated enzyme, telomerase, in malignant tumors maintain the telomere length shortened during cell replication. In contrast, in normal somatic cells, the mortality is increased via one of the p53 functions produced by a signal linked to critically shortened telomere region. In this study, wild type p53 gene was introduced into the established cell line using a lipofectin method. Then it was examined whether wild type p53 plays a role in regulation of the TA, human telomerase reverse transcriptase (hTERT) protein production and in hTERT mRNA expression. The cells derived from a tongue squamous cell carcinoma had two point mutation of p53 and TA, hTERT mRNA expression and hTERT production detected as protein were examined by the methods of telomerase repeat amplification protocol (TRAP), reverse transcriptase (RT)-PCR and western blotting methods, respectively. In the present series of studies, TA, hTERT mRNA expression and hTERT revealed a down regulation at 24 and 48 hours after wild type p53 introduction. Our findings suggest that wild type p53 down regulates TA and hTERT production as protein via repression of hTERT transcription.
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