| Project/Area Number |
25830111
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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
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| Research Institution | Kanazawa University |
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Principal Investigator |
NAKATA Asuka 金沢大学, がん進展制御研究所, 助教 (70597921)
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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 |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 肺腺癌 / イレッサ / 肺癌 / イレッサ耐性 / 肺がん / gefitinib / EGFR-TKI |
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| Outline of Final Research Achievements |
Although Iressa (gefitinib) were greatly effective in lung adenocarcinoma patients harboring EGFR mutations, these patients ultimately have acquired resistance to gefitinib. To explore novel molecular mechanisms for gefitinib-resistance, we established the gefitinib-resistant PC9M2 cells that were spontaneously derived from gefitinib-sensitive PC9. Microarray analysis revealed that β－catenin-related genes were upregulated in PC9M2 cells compared with PC9 cells. We next demonstrated that the downregulation of β-catenin partially restored the sensitivity to gefitinib in PC9M2 cells. Using the tissues from lung cancer patients harbored EGFR mutation, we showed that activation of β-catenin was related with gefitinib sensitivity in patient’s samples, suggesting that enhanced β-catenin activation is associated with primary and acquired resistance to gefitinib. Targeting β-catenin pathway may be useful for overcoming the resistance to gefitinib
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