Project/Area Number |
18591761
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Urology
|
Research Institution | Kagoshima University |
Principal Investigator |
NAKAGAWA Masayuki Kagoshima University, Graduate School of Medical and Dental Sciences, Professor (90164144)
|
Co-Investigator(Kenkyū-buntansha) |
ENOKIDA Hideki Kagoshima University, Graduate School of Medical and Dental Sciences, Senior Assistant Professor (80347103)
|
Project Period (FY) |
2006 – 2007
|
Project Status |
Completed (Fiscal Year 2007)
|
Budget Amount *help |
¥3,920,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥420,000)
Fiscal Year 2007: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2006: ¥2,100,000 (Direct Cost: ¥2,100,000)
|
Keywords | gene methylation / urothelial cancer / bladder cancer / tumor suppressor gene / methylation score / prediction of prognosis / collagen type 1 A2 / p16INK4a / p14ARF / DNA microarray法 / 細胞周期関連遺伝子 |
Research Abstract |
Purpose : Many genes responsible for the bladder cancer progression have been isolated recently. We have reported that hypermethylation of 2 tumor suppressor genes, pl6INK4a and p14ARF is involved in poor prognosis and tumor invasiveness in patients with bladder cancer. In the present study, we examined methylation status of collagen 1A2 gene promoter region in terms of prediction of patient prognosis. Materials and Methods : We examined methylation status of collagen 1A2 gene in the presence and absence of demethylation agent, 5 aza-cytizine in human BOY cultured bladder cancer cells. We examined the frequency of methylation of collagen 1A2 gene in 97 clinical specimens from radical cystectomy and TURBT. Furthermore, we transfected collagen 1A2 gene into human bladder cancer cells and examined cell migration ability and growth rate in both transfectants and control cells. Results : Gene expression of collagen 1A2 gene was increased by 5 aza-cytizine treatment. Collagen 1A2 gene expression in bladder tumors was significantly lower than that in normal bladder tissues. Methylation scores in the bladder tumors are significantly higher that those in normal bladder tissues. Cell migration and growth rate in collagen 1A2 gene transfectants are significantly decreased compared to those in control cells. Conclusions : Collagen 1A2 gene expression is suppressed by the promoter methylation in human bladder cancers. These results suggest that collagen 1A2 gene plays a role in tumor suppressor in human bladder cancer.
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