Analysis for molecular mechanism of SFN-induced lung adenocarcinoma progression
| Project/Area Number |
26860230
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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 |
Human pathology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
Shiba Aya 筑波大学, 医学医療系, 助教 (50708427)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 肺腺癌 / 初期悪性化 / Stratifin / SKP1 / stratifin / リン酸化cyclin E1 / トランスジェニックマウス |
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| Outline of Final Research Achievements |
Here, we performed an in vivo and in vitro study to clarify the role of SFN and the underlying molecular mechanism in progression of lung adenocarcinoma.
First, we generated SFN-transgenic mice showing lung-specific expression of human SFN. We found that Tg -SFN developed lung tumors at a significantly higher rate than control mice.
One of the SFN-binding proteins, SKP1 is an adapter component of E3 ubiquitin ligase, forming a SCF complex. Our SKP1 IHC and previous results indicate that SFN combines with SKP1 and blocks SCF complex function. We already identified the SFN binding domain in SKP1 protein using in silico simulation, and started screening for small molecule compounds that specifically bind to SFN. Targeted therapy to block the SFN-SKP1 combination might be a new treatment strategy for patients with lung adenocarcinoma.
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Report
(3 results)
Research Products
(4 results)
