| Project/Area Number |
26861088
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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 |
Digestive surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Research Collaborator |
HIGASHI Takaaki 熊本大学, 大学院生命科学研究部, 大学院生
KUROKI Hideyuki 熊本大学, 医学部附属病院, 非常勤診療医師
BEPPU toru 熊本大学, 医学部附属病院, 特任助教
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 肝内胆管癌 / 上皮間葉転換 / Integrin-β6 / 癌細胞浸潤 / 癌細胞増殖 / TGF-β-Smadシグナル / EMT / cholangiocarcinoma / TGF-β |
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| Outline of Final Research Achievements |
ICC is characterized as a poor prognostic disease represented by the highly invasiveness. EMT plays a pivotal role in cancer invasion and metastasis, and then TGF-β signaling is a potent inducible factor of EMT. Integrin-β6, which is an epithelial restricted trans-membrane protein, promotes binding to extracellular matrix proteins. In this study, we investigated the role of integrin-β6 during TGF-β-mediated EMT using ICC cell lines, and examined the clinic-pathological significance of Integrinβ6 expression in ICC patients.
Addition of TGF-β to ICC cells successfully induced EMT, spindle-shaped morphology, and high invasiveness, with the integrin-β6 induction. The inhibition of integrin-β6 expression using RNAi abolished TGF-β-mediated EMT induction. In clinical setting, high integrin-β6 expression was significantly associated with Stage IV, lymph node metastasis, and then resulted in worse prognosis compared with low expression group.
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