| Project/Area Number |
07671707
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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 | Gunma University |
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Principal Investigator |
FUKABORI Yoshitatsu Gunma University School of Medicine, Research Associate, 医学部, 助手 (90199167)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1995: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | prostate cancer / hormone / androgen / dependent / FGF / growth factor / FGFR / KGF / レセプター / ホルモン依存性 / splice variant |
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| Research Abstract |
The prostatic tissues were gotten by 18 gauge needle from the patients at the biopsy for prostatic cancer. The tissues were prepared for the detection of Fibroblast Growth Factor Receptor 2 IIIb (FGFR2IIb), FGFR2IIIc and FGF2 messages. The expressions of these messages were detected by RT-PCR.FGFR2IIIb, FGFR2IIIc and FGF2 messages were found in 6,6 and 7 out of 7 prostate cancer patients newly diagnosed, respectively. All of 3 messages were found in 10 patients specimens of recurrent prostatic cancer and in 8 patients specimens of benign prostatic hyperplasia. All of three genes were expressed in both metastatic lesions of liver and bone tissues from an autopsy case which died of recurrent prostatic cancer. Expression of FGFR2IIIb was found in LNCaP cells and human prostatic epithelial cells (HPE). FGFR2IIIb expression was negative in PC-3 cells and human prostatic smooth muscle cells (HPSMC). FGFR2IIIc expression was positive in LNCaP,PC-3 and HPE.FGFR2IIIc expression was negative in HPSMC.FGF2 expression was positive in PC-3, HPE and HPSMC.FGF2 was negative in LNCaP.Expression of KGF/FGF-7 was detected in all tissues and cells which contain prostatic stromal cells.
These results suggested that LNCaP cells may proliferate reacting to KGF/FGF-7 as andromedin when they are alive together with prostatic stromal cells. The loss of the expression of FGFR2IIIb may be responsible for androgen independency of PC-3 which may not respond to KGF/FGF-7 as andromedin. There is a possibility that PC-3 cells got malignant progression by the autocrine mechanism of FGF2-FGFR2IIIc reaction. The tissue specimens from biopsies and autopsy revealed that candidate androgen-independent cells may exist at the early stage of prostate cancer. The tissue specimens from BPH may indicate that androgen-independent normal cells are responsible for the candidate androgen-independent prostate cancer cells.
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