| Project/Area Number |
21790793
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Gunma University (2010)
Shizuoka Cancer Center Research Institute (2009) |
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Principal Investigator |
KAIRA Kyoichi Gunma University, 医学部, 医員 (40400783)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | アミノ酸トランスポーター / 肺癌 / 予後因子 / 抗腫瘍効果 / 非小細胞肺癌 / 化学療法 / LAT1 / LAT1阻害剤 / mTOR / FAMT-PET / gefitinib / 治療 / 予後 |
|---|
| Research Abstract |
L-type amino acid transporter 1 (LAT1) is highly expressed in various neoplasms. Antitumor activity of inhibiting LAT1 was analyzed in non-small cell lung cancer (NSCLC). Expression of LAT1 mRNA in 54 lung cancer cell lines was examined by RT-PCR. An inhibitor of LAT1, 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH), was administered to H1395 cell. LAT1 expression was examined in correlation with clinical features and outcome in 120 NSCLC patients. Inhibition of LAT1 by BCH reduced cell viability in H1395 cells. Furthermore, co-administration of gefitinib with BCH reduced the viability of the cells more than either agent alone. Inhibition of LAT1 reduced the level of phosphorylation of mTOR, p70S6K and 4EBP1. LAT1 protein expression was closely associated with wild type EGFR, and was an independent significant factor to predict a poor prognosis. Inhibition of LAT1 may be a new rationale to the effective therapy of NSCLC without EGFR mutation.
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