Molecular basis of the oncogenic effects of novel oncogene candidates, TRB family members
| Project/Area Number |
15K07937
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Nagoya City University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | TRB3 / TRB1 / p53 / EMT / TGF-beta / がん幹細胞 / FOXO1 / CD44 / FoxO1 / PGC-1alpha / TGF-b / Foxo1 / HDAC1 |
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| Outline of Final Research Achievements |
Overexpression and/or dysfunction of TRB1/TRB3, mammalian orthologues of Drosophila Tribbles, which regulates differentiation and development, is supposed to participate in the oncogenesis, and they possess characteristics of oncogene. However the precise molecular mechanism remains poorly understood. In this study, we evaluated this hypothesis.
We demonstrated that TRB1 inhibited the transcriptional activity of typical tumor suppressor genes, p53 and FOXO1, to accelerate the proliferation of tumor cells. TRB1 is also one of the proteins responsible for the maintenance of cancer stem cell characters, and the induction of the epidermal-mesenchymal transition (EMT) to activate the invasion and metastasis of cancers, and to acquire the resistance against several anticancer drugs. These results suggested that TRB1 fully participated in the oncogenesis and malignant progression.
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Report
(4 results)
Research Products
(62 results)
