Project/Area Number |
20591633
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Digestive surgery
|
Research Institution | Kumamoto University |
Principal Investigator |
SUGITA Hiroki Kumamoto University, 医学部附属病院, 非常勤診療医師 (30398218)
|
Co-Investigator(Kenkyū-buntansha) |
TAKAMORI Hiroshi 熊本大学, 大学院・生命科学研究部, 講師 (90363514)
HIROTA Masahiko 熊本大学, 医学部附属病院, 非常勤診療医師 (80284769)
KAMOHARA Hidenobu 熊本大学, 医学部附属病院, 講師 (90398222)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | insulin / IGFシグナル / 癌 / 一酸化窒素(NO) / ユビキチン化 / IGF-I / IRS-1 / Akt/PKB / 膵癌 / EGF / MEK / Akt / PKB / 一酸化窒素 |
Research Abstract |
NO inhibits the phosphorylation of IGF-IR, EGFR, Akt and IRS-1 protein expression, but upregulates Ras/Erk pathway in cancer cells (pancreatic and colon cancer cells). C terminus is responsible site for NO-induced ubiqutination and degradation of IRS-1 protein. NO inhibits the proliferation and invasion of pancreatic, colon and breast cancer cells. Combination of NO-donor and MEK-inhibitor enhances anti-cancer activity in these cancer cells.
|