| Project/Area Number |
19390104
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Nara Medical University |
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Principal Investigator |
KONISHI Noboru Nara Medical University, 医学部, 教授 (20145832)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMADA Keiji 奈良県立医科大学, 医学部, 講師 (90336850)
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| Project Period (FY) |
2007 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥9,750,000 (Direct Cost: ¥7,500,000、Indirect Cost: ¥2,250,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2008: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2007: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
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| Keywords | 前立腺 / 癌化 / 組織幹細胞 / senescence / transient amplifying cell / junB / tranint amlifying cell |
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| Research Abstract |
Transient amplifying (TA) cells are a subset of basal cell populations within the prostate from which cancers are thought to originate. Most TA cell populations showed increased expression of p53, p21, p16, and pRb, resulting in senescence. However, TA cell clones with reduced p16 expression successfully bypassed this phase. The close correlation was found between the levels of junB and p16 expression. Transfection of junB siRNA in prostatic TA cells allowed the cells to escape senescence, presumably through inactivation of p16/pRb ; this suggests that activation of junB/p16/pRb is required to block clonal expansion. Interestingly, the percentage of peripheral zone TA cells evading senescence was significantly higher than those from central and transition zones. Metastatic prostate tumors, as well as prostate cancers with high Gleason scores, demonstrated significantly low junB immunopositivity. junB thus apparently plays an important role in controlling prostate carcinogenesis and may be a new target for cancer prevention and therapy.
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