| Project/Area Number |
23790902
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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 |
Respiratory organ internal medicine
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| Research Institution | Kanazawa 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)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 肺癌 / 分子標的治療 / EGFR変異 / 足場蛋白質 / 薬剤耐性 / EGFR / がん分子標的 / 上皮成長因子受容体 |
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| Research Abstract |
We focused on Akt kinase-interacting protein1 (Aki1), a scaffold protein of PI3K /PDK1/Akt, and assessed its role in EGFR mutant lung cancer. Aki1 constitutively associates with mutant EGFR in lung cancer cells. Silencing of Aki1 inhibited cell growth of EGFR mutant lung cancer cells and induced apoptosis of them. Treatment with Aki1 siRNA dramatically inhibited growth of EGFR mutant lung cancer cells in a xenograft model. Moreover, Aki1 was frequently expressed in tumor cells of EGFR mutant lung cancer patients, including those with acquired resistance to EGFR-TKI treatment. Our data suggest that Aki1 may be an ideal target for EGFR mutant lung cancer patients, especially those with acquired EGFR-TKI resistance due to EGFR T790M gatekeeper mutation.
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