CCL2 induced by RB inactivation contributes to the formation of tumor-promoting inflammatory microenvironment
| Project/Area Number |
25830077
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | RB / CCL2 / CCR2 / Tumor microenvironment / Rb / IL-6 / Breast cancer |
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| Outline of Final Research Achievements |
Inactivation of RB gene is frequently found during tumor progression and correlated with drug resistance or undifferentiated state in some kinds of cancer. We previously found that RB inactivation contributes to the acquisition of stem cell-like activity via activation of inflammatory signaling. But the receptors of some cytokines induced by RB inactivation such as CCL2 were not expressed in tumor cells themselves. Up-regulation of CCL2 secretion was dependent on ROS accumulation and subsequent JNK activation caused by RB inactivation. RB inactivated myofibrosarcoma cells highly expressed CCL2. And these cells showed higher tumorigenic activity in wild type mice but not in CCR2 knockout mice. Angiogenesis and infiltration of Gr-1 positive cells into tumor microenvironment were decreased in CCR2 knockout mice compared with wild type mice. Here we state that CCL2 induced by RB inactivation contributes to the formation of tumor-promoting inflammatory microenvironment.
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Report
(3 results)
Research Products
(9 results)
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[Journal Article] Undifferentiated State Induced by Rb-P53 Double Inactivation in Mouse Thyroid Neuroendocrine Cells and Embryonic Fibroblasts2015
Author(s)
Kitajima S, Kohno S, Kondoh A, Sasaki N, Nishimoto Y, Li F, Mohammed MS, Muranaka H, Nagatani N, Suzuki M, Kido Y, Takahashi C
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Journal Title
STEM CELLS
Volume: -
Issue: 5
Pages: 1657-1669
DOI
Related Report
Peer Reviewed / Acknowledgement Compliant
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[Journal Article] ATM mediates pRB function to control DNMT1 protein stability and DNA methylation.2013
Author(s)
Shamma A, Suzuki M, Hayashi N, Kobayashi M, Sasaki N, Nishiuchi T, Doki Y, Okamoto T, Kohno S, Muranaka H, Kitajima S, Yamamoto K, Takahashi C
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Journal Title
Molecular and Cellular Biology
Volume: 33
Issue: 16
Pages: 3113-3124
DOI
NAID
Related Report
Peer Reviewed
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