Investigation of the participation in anticancer agent tolerance of microRNA in oral cancer
| Project/Area Number |
23792369
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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 |
Surgical dentistry
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| Research Institution | Nara Medical University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 5-FU / BRCA2 / UCN / microRNA |
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| Research Abstract |
Using cells derived from DNA repair enzyme deficiency Chinese hamster lung fibroblast, we investigated the target candidate what raised cytotoxicity reaction of 5 -FU in the DNA repair course. We measured a survival rate and the measurement of the quantity of DNA double-strand break using BRCA2 deficient cells derived from Chinese hamster lung fibroblast and ku80 deficient cells and each parent root cell. As a result, the BRCA2 deficient cells accepted the cytotoxicity reaction that had high approximately 2.5 times by 5-FU. Furthermore, with the BRCA2deficient cells, the repair delay of the DNA double-strand break to result from 5-FU treatment as compared with the parent root cells was confirmed.As an additional experiment, we confirmed a sensibilization effect of 5-FU using the SAS cells which were cells and the tongue cancer cells of the Chinese Hamster Lung Fibroblast (BRCA2 wild-type) origin using UCN which was BRCA2 and the Chk1 inhibitor with the relation. A low bottom significantly accepted the survival rate of cells by using UCN together as compared with 5 -FU use alone in both cells. In other words we were able to achieve sensitivity of 5-FU by inhibiting homologous recombination restoration.
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Report
(3 results)
Research Products
(3 results)
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[Journal Article] Depression of p-53-independent Akt survival signals in human oral cancer cells bearing mutated p53 gene after exposure to high-LET radiation2012
Author(s)
Yousuke Nakagawa, Akihisa Takahashi, Athuhisa Kajihara, Nobuhiro Yamakawa, Yuichiro Imai, Ichiro Ota, Noritomo Okamoto, Eiichiro Mori, Taichi Noda, Yoshiya Furusawa, Tadaaki Kirita, Takeo Ohnishi
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Journal Title
Biochemical and Biophysical reserch Communications
Volume: 423
Pages: 654-660
Related Report
Peer Reviewed
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