| Project/Area Number |
23590194
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Medical pharmacy
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| Research Institution | Tohoku Pharmaceutical University |
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Principal Investigator |
YOMOGIDA Shin 東北薬科大学, 薬学部, 講師 (80230845)
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| Co-Investigator(Kenkyū-buntansha) |
SOMEYA Akimasa 順天堂大学, 医学部, 准教授 (90167479)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | がん / 抗がん剤耐性 / P-糖タンパク質 / ARF-GEP100 / ARF6 / Doxorubicin / 癌 / がん細胞 / 耐性マーカー / ドキソルビシン / ABCトランスポーター |
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| Research Abstract |
It has been already revealed that ARF-GEP100 (p100) preferentially activates ARF (ADP-ribosylation factor) in vitro and regulated various cell functions. In contrast, P-glycoprotein (Pgp) transports a broad range of anticancer drugs out of the cells. The inhibition of Pgp is expected to circumvent the Pgp-mediated drug resistance. In this study, we examined whether p100 may affect the expression of Pgp using the Doxorubicin (DOX)-resistant K562 cells. The expression level of p100 increased, accompanied with Pgp expression. Interestingly, the expression of p100 was increased in the cell membrane fraction. Furthermore, anti-Pgp antibody immunoprecipitated p100 in DOX resistant cell lysate. The DOX resistant cells treated with ARF6 siRNA were investigated for expression level of Pgp and p100. However, the expression of Pgp and p100 was not changed.
Collectively, these observations suggest that p100 may be involved in the expression and activation of Pgp to induce the DOX resistance.
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