Investigation of novel molecular mechanisms associated with the metastasis of epidermal growth-factor receptor-tyrosine kinase inhibitor-resistant non-small cell lung cancer
| Project/Area Number |
25871225
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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 |
Tumor therapeutics
Tumor biology
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| Research Institution | Shizuoka Cancer Center Research Institute |
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Principal Investigator |
SERIZAWA Masakuni 静岡県立静岡がんセンター(研究所), その他部局等, 主任研究員 (00569915)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 非小細胞肺癌 / EGFR-TKI / EGFR-TKI耐性 / 転移 / 細胞遊走 / TGF-βシグナル / 細胞遊走能 / TGF-β / PPARγ / CRKL |
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| Outline of Final Research Achievements |
The aim of this study was to investigate the molecular mechanisms relevant to metastasis after the acquisition of epidermal growth-factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) resistance in non-small cell lung cancer (NSCLC). We previously reported that EGFR-TKI-resistant PC-9ER cells, established from PC-9 NSCLC cells with an EGFR-activating mutation, show enhanced motility via transforming-growth factor (TGF)-β2-induced activation of the TGF-β pathway. Therefore, we focused on the identification of the gene alterations associated with the activation of TGF-β pathway in PC-9ER cells with omics-technologies. Our data indicated that amplification of the CRKL gene, which is known to associate with TGF-β pathway, occurred in PC-9ER cells. Moreover, 19 PC-9ER-specific mutations were detected in 13 genes associated with cell motility and invasion. Further studies are required to characterize the effects of these gene alterations on metastasis in EGFR-TKI-resistant NSCLC cells.
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Report
(3 results)
Research Products
(3 results)
