| Project/Area Number |
24890289
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | Okinawa Institute of Science and Technology Graduate University |
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Principal Investigator |
YO-TARO Shirai 沖縄科学技術大学院大学, 細胞シグナルユニット, 研究員 (30630545)
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| Project Period (FY) |
2012-08-31 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 癌 / デアデニレース / mRNA / 発現制御 / 病理学 |
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| Research Abstract |
The relationship between the mRNA turnover dysfunction and the cancer progression is not well understood. I found that knockdown of CNOT3 in lung cancer cells by DOX-induced shRNA attenuates their proliferation. In addition, the expression level of other CCR4-NOT components was decreased by knockdown of CNOT3 at protein level. Currently, I am searching for the target genes of CNOT3 which are responsible for this growth inhibition of lung cancer cells by microarray analysis.
In addition, I established the lung cancer cells in which CNOT3 is stably overexpressed. I am going to evaluate whether CNOT3 affects the motility and invasiveness of lung cancer cells, and also metastasis using xenograft model.
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