| Project/Area Number |
15K19070
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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 |
Experimental pathology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
OKITA Yukari 筑波大学, 医学医療系, 研究員 (30743710)
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| Research Collaborator |
KATO Mitsuyasu 筑波大学, 医学医療系, 教授 (20194855)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | MafK / GPNMB / 腫瘍形成 / EMT / 転移形成 / 分子標的治療 / Gpnmb / 環状ペプチド |
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| Outline of Final Research Achievements |
Previously we showed that the transcription factor MafK is involved in induction of epithelial-mesenchymal transition (EMT) and malignant progression of breast cancer cells. Furthermore, we identified glycoprotein nmb (GPNMB) as a target of MafK, which also has the functions as an inducer of EMT and tumorigenesis.
In this project, we further investigated the molecular mechanisms how MafK-GPNMB axis contributes to EMT induction and tumorigenesis. Then, we found post-translational modification of MafK is important for functional regulation of MafK in EMT induction and tumorigenesis. Moreover, we identified some domains or motifs which are essential for GPNMB-mediated EMT induction and tumorigenesis. We are going to investigate further detail mechanisms in order to find new target for breast cancer treatment.
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