Molecular mechanisms coordinating between cell cycle and differentiation in lung epithelial cells
| Project/Area Number |
20590928
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kumamoto University |
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Principal Investigator |
FUJIMOTO Tetsuhiro Kumamoto University, 大学院・生命科学研究部, 助教 (70359818)
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| Co-Investigator(Kenkyū-buntansha) |
ITO Takaaki 熊本大学, 大学院・生命科学研究部, 教授 (70168392)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 細胞周期 / 細胞癌化 / cyclin D1 / RUNX3 / p21 / 転写制御 / cvclin D1 / 肺上皮細胞 / Cyclin D1 / 肺腺癌 |
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| Research Abstract |
Transcriptional function of cyclin D1, whose deregulation is frequently observed in human cancers, has been suggested to contribute to cancer formation. We show that cyclin D1 protein inhibits RUNX3 activity by directly binding to it andB interfering with its interaction with p300 interaction in lung cancer cells. Cyclin D1 inhibits p300-dependent RUNX3 acetylation and negatively regulates cyclin-dependent kinase (cdk) inhibitor p21 expression. These transcriptional effects of cyclin D1 do not require cdk4/6 kinase activation. We propose that cyclin D1 provides a transcriptional switch that allows the tumor suppressor activity of RUNX3 to be repressed in cancer cells.
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Report
(4 results)
Research Products
(8 results)
