| Project/Area Number |
18591775
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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 |
Urology
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
KURUMA Hidetoshi Jikei University School of Medicine, School of Medicine, Research Associate (80327329)
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| Co-Investigator(Kenkyū-buntansha) |
EGAWA Shin The Jikei University, School of Medicine, Professor (60160347)
TAKAHASHI Hiroyuki The Jikei University, School of Medicine, Assistant Professor (00246414)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,010,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | cancer / Protein / Biomarker / 蛋白質 |
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| Research Abstract |
Using high molecular weight proteomic analysis, we previously showed that Staphylococcal nuclease domain-containing protein 1 (SND1) is highly expressed in recurrent androgen insensitive prostate cancer tissues. The objective of this study was to further characterize SND1 expression and to investigate its biological potential in prostate cancer. Radical prostatectomy specimens were obtained from 62 prostate cancer patients. Immunohistochemical staining patterns of SND1 were evaluated using an in-house polyclonal antibody. We confirmed expression of SND1 mRNA in prostate cancer cells using an in situ hybridization technique. To determine its biological functions, we investigated cell growth by MTT assay in vitro using siRNA treatment. SND1 was expressed in small granular structure patterns in cytoplasm in 60 of 62 prostate cancers (97%). It was highly expressed in prostate cancer and high grade prostatic intraepithelial neoplasm (HGPIN) compared with hyperplasia and normal epithelium (p<0.0001). Its expression was found to be more intense in cancers with higher grade (p=0.025) and higher prostate specific antigen (PSA,p=0.012), respectively, reflecting a more aggressive phenotype. SND1 mRNA was overexpressed in cancer cells, and the growth activity was suppressed in SND1 knocked down cells. In conclusion, SND1 expression intensity was found parallel to the dedifferentiation status of prostate cancer cells, thus reflecting a more aggressive phenotype. SND1 may have a pivotal role in cell growth in prostate cancer since its endogenous RNA interference regulated cell growth. SND1 may be a promising potential biomarker and therapeutic target for prostate cancer.
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