| Project/Area Number |
25460384
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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 |
Pathological medical chemistry
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SHIBATA Kiyoshi 浜松医科大学, 光尖端医学教育研究センター, 技術専門員 (80397372)
FUJIE Michio 浜松医科大学, 光尖端医学教育研究センター, 技術補佐員 (90397373)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥260,000 (Direct Cost: ¥200,000、Indirect Cost: ¥60,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 分子標的薬 / LIX1L蛋白質 / 胃癌 / miRNA / LIX1L / RNA結合蛋白質 / 癌細胞 / 標的分子 / チロシンキナーゼ阻害 / ペプチド / プロテオーム解析 / シグナル伝達 |
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| Outline of Final Research Achievements |
We identified the LIX1L, which specifically expressed in various cancer cells, as a novel marker for cancer. Its function is unknown in detail. In this study, we revealed that LIX1L promoted cancer cell proliferation both in vitro and in vivo. ROS1 kinase phosphorylates 136th Tyrosin in LIX1L, and LIX1L subsequently induces proliferates cancer cells via binding to various RMA including miRNA. We also found peptide, which specifically inhibited the function of LIX1L, and the peptide inhibited gastric cancer cell proliferation as a decay. Therefore, we revealed that LIX1L was specifically expressed in various cancer cells, and the PY136 peptide, which targeted to LIX1L amino acid sequence including 136th Tyrosin, has a possibility as a new molecular targeted agent for cancer therapy in LIX1L expressed cancer cells.
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