2015 Fiscal Year Final Research Report
Study on the molecular mechanism of intracellular energy of thyroid follicular cancer cells and development of new therapeutic strategy for thyroid cancer
| Project/Area Number |
25870489
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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 |
Endocrinology
Tumor therapeutics
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| Research Institution | Kochi University |
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Principal Investigator |
Taguchi Takafumi 高知大学, 教育研究部医療学系臨床医学部門, 講師 (40437710)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 甲状腺 |
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| Outline of Final Research Achievements |
The present research demonstrated that the co-transfected SRC-1 increased transcriptional activity of PPARγ and PAX8-PPARγ on the AQP7 promoter in the presence of ciglitizone. On the other hand, co-transfected PGC-1 strongly upregulated PAX8-PPARγ transcriptional activity on the AQP7 promoter even in the absence of ciglitizone. We confirmed that these transcriptional effects depend primarily on the presence of the PPARγ DNA binding domain (DBD), such that either mutation of the PPARγ DBD in PAX8-PPARγ, or mutation of the putative PPARγ response element, was sufficient to abolish PAX8-PPARγ-mediated regulation of the AQP7 promoter. We conclude that PAX8-PPARγ has strong ligand-independent activity on AQP7 transcription that may be mediated via its interaction with PGC-1α and that ligand-dependent activity may be mediated via SRC-1 recruitment.
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| Free Research Field |
内分泌
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