| Project/Area Number |
22590700
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
TAKAYAMA Tetsuji 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 教授 (10284994)
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| Co-Investigator(Kenkyū-buntansha) |
OKAMURA Seisuke 徳島大学, 大学院・ヘルスバイオサイエンス 研究部, 助教 (30274210)
KAJI Masako 徳島大学, 大学院・ヘルスバイオサイエンス 研究部, 助教 (30518220)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 下部消化管学(小腸、大腸) / 大腸癌 / GST-π / RAF / JNK / K-ras / 大腸発癌 / MAP kinase |
|---|
| Research Abstract |
We investigated the role of GST-πin growth promotion and apoptosis resistance of colorectal cancer. When a mutated K-ras gene was transfected into K-ras wild colon cancer cell line, GST-πexpression was induced. The transfectant cells showed enhanced growth promotion activity via RAF/MEK/ERK activation and apoptosis resistance by inhibited JNK and p53 pathway. In contrast, GST-πknockdown cells showed growth inhibition and apoptosis enhancement by the inverse action mechanisms. Immunoprecipitation revealed that GST-πwas directly interacted with RAF and JNK respectively. These results indicate that GST-π promote cell growth via direct binding to RAF and subsequent RAF/MEK/ERK activation, and inhibit apoptosis via direct binding to JNK and subsequent p53 apoptosis pathway.
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