| Project/Area Number |
20590361
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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 |
Human pathology
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| Research Institution | Akita University |
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Principal Investigator |
YOSHIOKA Toshiaki Akita University, 医学部, 助教 (80302264)
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| Co-Investigator(Kenkyū-buntansha) |
OMORI Yasufumi 秋田大学, 大学院・医学系研究科, 准教授 (90323138)
ENOMOTO Katsuhiko 秋田大学, 大学院・医学系研究科, 教授 (20151988)
YAMAMOTO Yohei 秋田大学, 大学院・医学系研究科, 助教 (70400512)
NISHIKAWA Yuji 秋田大学, 大学院・医学系研究科, 准教授 (90208166)
YOSHIDA Masayuki 秋田大学, 医学部, 助教 (40451645)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 分子病理 / インテグリンベータ4 / ヒト前立腺癌 / インテグリンβ4 / ErbB2 / Met / 遊走能 / 浸潤能 / 増殖能 / アポトーシス |
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| Research Abstract |
In this study, we hypothesized that integrin β4 (β4) may promote the progression of the human prostate cancer. To examine the hypothesis, we studied first, the role of β4 in the human prostate cancer cells, DU145 and LNCap. Second, we tested the expression of β4 and other molecules, which were concerned to β4, in the human prostate cancer tissues. In the human prostate cancer cells, β4 bonded ErbB2 and c-Met and made the cells increase proliferation and invasion, and decrease to get into apoptosis in vitro by reinforcing tyrosine-phosphorylation of ErbB2 and c-Met. β4 also increased the size of the xenograft under the skin, in vivo. Immunohistochemical staining of β4 on human prostate cancer tissues revealed that positive expression of β4 was found more than half of the samples. Interestingly, many of β4 positive cancer cells also expressed ErbB2 and c-Met. These results indicate that β4 may promote the progression of human prostate cancer by cooperating with ErbB2 and Met signaling.
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