| Project/Area Number |
20790974
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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 |
Digestive surgery
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| Research Institution | Nippon Medical School |
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Principal Investigator |
YAMAMOTO Tetsushi Nippon Medical School, 医学部, 助教 (20453920)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2008: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | ケラチノサイト増殖因子 / ルミカン / 膵臓癌 / ヒト胎児腎細胞 / 細胞増殖 / プロテオグリカン / ERKシグナル / AKTシグナル |
|---|
| Research Abstract |
Keratinocyte growth factor (KGF) and its receptor, KGFR play important roles in cell growth and invasion in pancreatic cancer. Administration of recombinant KGF to pancreatic cancer cell lines induced cell growth by does-dependent manner, and it also activated ERK and p38, a member of MAPK. Lumican belongs to the proteoglycan family. When we regulated lumican expression levels in pancreatic cancer cell line, we found that there is a positive correlation between lumican expression levels and cell growth, ERK activation. Proteoglycan plays an important role in stabilizing the binding of KGF and KGFR. Therefore, lumican may regulate pancreatic cancer cell growth to regulate KGF/KGFR signaling pathway.
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