| Project/Area Number |
26293302
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Kyoto University |
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Principal Investigator |
SHIMADA Yutaka 京都大学, 薬学研究科(研究院), 教授 (30216072)
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| Co-Investigator(Kenkyū-buntansha) |
清水 一治 京都大学, 薬学研究科(研究院), 教授 (50456836)
武井 義則 京都大学, 薬学研究科(研究院), 講師 (30502455)
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| Co-Investigator(Renkei-kenkyūsha) |
ITOU Yuji 鹿児島大学, 理工学研究科, 教授 (60223195)
TUCHIYA Soken 熊本大学, 生命科学研究部, 講師 (80423002)
MARUSAWA Hiroyuki 京都大学, 医学(系)研究科, 講師 (80324630)
OHTSUJI Eigo 京都府立医科大学, 医学(系)研究科, 教授 (20244600)
TSUKADA Kazuhiro 富山大学, 医学薬学研究部(医学), 教授 (90171967)
MATSUMOTO Osamu 千葉科学大学, 薬学部, 教授 (10231599)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,250,000 (Direct Cost: ¥12,500,000、Indirect Cost: ¥3,750,000)
Fiscal Year 2016: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥8,450,000 (Direct Cost: ¥6,500,000、Indirect Cost: ¥1,950,000)
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| Keywords | 癌 / FGFRL1 / 食道癌 / 抗体治療 / 抗体作成 |
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| Outline of Final Research Achievements |
We identified fibroblast growth factor receptor like-1 (FGFRL1) as the main prognostic factor among 5 different FGFR receptors. The Duolink method revealed that FGFRL1 formed heterodimers with FGFR1, 3, and 4 following an inoculation with FGF-2. The phage display method showed anti-FGFRL1 antibodies in the blood of esophageal cancer patients. We then newly established an anti-FGFRL1 monoclonal antibody that inhibits (80%) the growth of several esophageal cancer cell lines in vitro.
We established two FGFRL1 knockout cells (KO15 and KO21). These cells reduced actin fragments, resulting in growth suppression not only in vitro, but also in vivo. A histological examination revealed that in contrast to parental cells, FGFRL1 knockout cells exhibited the ability to differentiate. Furthermore, the expression of MMP-1 was markedly suppressed in knockout cells. Our results demonstrate that anti-FGFRL1 treatments represent a promising strategy for esophageal cancer.
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