Analysis of abnormal DNA structure and down regulation of a new tumor suppressor, FEZ1 gene, in oral squamous cell carcinoma.
| Project/Area Number |
12671925
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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 | Tokyo Dental College (2002)
Chiba University (2000-2001) |
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Principal Investigator |
YAMA Mitsuru Tokyo Dental College, Department of Dentistry, Lecturer, 歯学部, 助手 (60230299)
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| Co-Investigator(Kenkyū-buntansha) |
TANZAWA Hideki Chiba University, Graduate School of Medicine, Professor, 大学院・医学研究院, 教授 (50236775)
相崎 邦男 (相崎 邦雄) 千葉大学, 医学部・附属病院, 助手 (50323423)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2002: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2001: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2000: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | Chromosome 8p22 / FEZ1 gene / tumor suppressor gene / oral cancer / methvlation / down-reeulation / demethvaktion / 5-aza-2'-deoxvcvtidine / 5-aza-2'deoxycytidine / 口腔扁平上皮癌 / 発現減弱・消失 / 第8番染色体 |
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| Research Abstract |
Allelic deletions on the short arm of chromosome 8 (8p) are frequent events inseveral human malignancies, including oral cancer. We have examined and found two common regions of deletion on 8p (8pl2, 8p22) in oral squamous cell carcinomas (SCC) s. The possible involvement of FEZl/LZTSl (FEZ1) gene, a candidate tumor suppressor gene, mapped at 8p22, was also evaluated. Here we analyzed whether FEZl alterations play arole in the development and progression of oral SCCs. In present study, we examined FEZ1 expression in 31 primary oral SCCs and 8 SCC-derived cell line by reverse transcription-PCR (RT-PCR). Thirty-five % of tumor (ll of 31) and 100% of cell lines (8 of 8) showed absent or reduced mRNA gene expression. Furthermore, to investigate the mechanism for silencing, cell were cultured with 5-aza-2'-deoxycytidine and all of cell linesshowed restoration by demethylating agent. These findings suggest that inactivation of the FEZ1 gene may contribute to the development of oral SCCs.
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Report
(4 results)
Research Products
(3 results)
