1998 Fiscal Year Final Research Report Summary
GROWTH MECHANISM OF BONE-METASTASIZED PROSTATIC CANCER
| Project/Area Number |
09671602
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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, Department of Urology, Assistant Professor, 医学部, 講師 (90199167)
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| Project Period (FY) |
1997 – 1998
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| Keywords | prostate carcinoma / bone metastasis / growth factor / BMP / KGF / FGF / real-time quantitative RT-PCR / osteoblastic growth |
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| Research Abstract |
It was demonstrated that KGF/FGF -7 and FGF-10 existed in the bone tissue. The expression of FGF-10 was higher than that of FGF-7. Prostatic cancer cell has the expression of FGFR2IIIb which is the receptor of FGF -7 and FGF-10. Some of the bone metastatic lesion expressed FGFR2IIIb (and FGFR2IIIc). No expression of FGFR2IIIb was found in the bone tissue. These results means that the growth of the prostatic cancer cell can be stimulated by these growth factors after their invasion into the bone tissue. Moreover, the expression of FGF-7 in metastatic lesion was higher than those in other bone tissue. These results suggest that the prostatic cancer cell may stimulate the expression of FGF-7 in bone stromal cells.
Primary culture of bone marrow stromal cells (BMSC) was established, Some of BMSCs were characterized as osteoblasts and the others were characterized as fibroblasts. The expression level of FGF-7 was significantly elevated at 10^<-12> M of DHT.DHT did not show a significant effect on the expression of FGF-10 or AR.There was a significant correlation between the expression levels of FGF-7 and AR.The message of FGFR2IIIb was detected in both local and bone lesion of prostate cancer.
These results suggest that the expression of FGF-7 in BMSC is controlled by androgen and the growth of prostatic cancer cells in bone-marrow is regulated by paracrine mechanism of FGF-7 as andromedin. There is a possibility that some parts of the bone lesions of the prostate cancer still have a potential of androgen responsiveness after recurrence against androgen ablation therapy.
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