2013 Fiscal Year Final Research Report
Molecular mechanism of cancer cell pluripotency responding to stress
| 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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| 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 |
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| 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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Research Products
(4 results)
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[Journal Article] Residual prostate cancer cells after docetaxel therapy increase the tumourigenic potential via constitutive CXCR4, ERK1/2 and c-Myc signalling loop activation2013
Author(s)
Hatano, K., Yamaguchi, S., Nimura, K., Murakami,K., Nagahara, A., Fujita, K., Uemura, M., Nakai, Y., Tsuchiya, M., Nakayama, M., Nonomura, N., and Kaneda, Y.
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Journal Title
Mol. Cancer Res
Volume: 11
Pages: 1088-100
DOI
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