| Project/Area Number |
18591755
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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 | Hiroshima University |
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Principal Investigator |
USUI Tsuguru Hiroshima University, Graduate School of Biomedical Sciences, Professor (30034060)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUBARA Akio Hiroshima University, Graduate School of Biomedical Sciences, Associate Professor (10239064)
YASUMOTO Hiroaki Hiroshima University, Graduate School of Biomedical Sciences, Assistant Professor (20314750)
TEISHIMA Jun Hiroshima University, Graduate School of Biomedical Sciences, Assistant Professor (20397962)
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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 |
¥3,880,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥480,000)
Fiscal Year 2007: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | prostate cancer / nuclear receptor / RIZ 1 / androgen receptor / transcriptional factor / DNA methylation / Guanine nucleotide binding protein / p53 |
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| Research Abstract |
1) Establishment of androgen independent prostate cancer cell line
We obtained the cell line that acquired the proliferation potency without androgen by culturing under charcoal stripped FBS for a long term. The anti-androgen medicine cannot show the growth inhibition effect in this cell line- We will analyze the cell line more closely in the future.
2) Analysis of DNA methylation of the RIZ1 gene in prostate cancer
Riz1 is a histone methyltransferase and a retinoblastoma protein-interacting zinc finger gene. DNA methylation of the RIZ1 gene was detected in 42.6% of prostate cancer tissues. DNA methylation of RIZ1 tended to be present more frequently in PCa specimens with a high Gleason score than in those with a low Gleason score. PC3 cell line showed loss of RIZ1 mRNA due to DNA methylation, and this loss was rectified by treatment with a demethylating agent, 5-Aza-2-deoxycytidine. These results suggest that transcriptional inactivation of RIZ1 by aberrant DNA methylation may contribute to prostate carcinogenesis.
3) Estrogen related receptor (ERR) and Guanine nucleotide binding protein-like3 (GNL3L)
We found out that the interaction between ERR and GNL3L. ERR and GNL3L express in prostate and prostate cancer tissue. GNL3L inhibits the transcriptional activity of ERR3 in prostate cancer cells. We will research a physiological function of ERRs and GNL3L in the prostate cancer cell in the future.
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