| Project/Area Number |
24659149
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Osaka University |
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Principal Investigator |
KANEDA Yasufumi 大阪大学, 医学(系)研究科(研究院), 教授 (10177537)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 癌幹細胞 / 抗がん剤耐性 / 前立腺がん / 多能性維持因子 / ストレス応答 / 抗癌剤耐性 / 前立腺癌 |
|---|
| Research Abstract |
Despite an increasing prevalence of patients with docetaxel refractory prostate cancer, little is known about its tumour biology. In this study, we demonstrated that the tumourigenic potential was increased in the docetaxel-resistant residual prostate cancer cells compared with the parental prostate cancer cells. An enhanced tumourigenic potential was controlled by the CXCR4, ERK1/2 and c-Myc signalling loop activation. Furthermore, the constitutive CXCR4, ERK1/2 and c-Myc signalling activation was demonstrated in clinical cancerous tissue samples from human patients with docetaxel-resistant prostate cancer. These signalling pathways may become treatment targets for inhibiting aggressive residual tumour cells after chemotherapy.
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