| Project/Area Number |
25871241
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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
Genome biology
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| Research Institution | Osaka City University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | TGF-beta / Proteomics / eIF signaling / metastatic mouse model / Breast cancer / プロテオミクス / 転移性乳がん / マウスモデル / 乳がん転移促進因子 / TGF-beta阻害剤 / 転移性乳癌モデル / 乳癌転移促進因子 |
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| Outline of Final Research Achievements |
Although TGF-β antagonists have been proposed as anti-metastatic therapies for patients with advanced stage cancer, how TGF-β mediates metastasis-promoting effects is poorly understood. In the present study, we found that systemic administration of the TGF-β receptor kinase inhibitor, SB-431542, significantly inhibited lung metastasis from transplanted 4T1 mammary tumors in Balb/c mice. The differentially expressed proteins in the comparison of lung metastases from SB-431542 treated and control vehicle-treated groups were analyzed by proteomics analysis. Our proteomic approach newly identified eIF pathway proteins as novel potential mediators of TGF-β tumor-promoting activity.
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