Study of mechanism of gastric carcinogenesis associated with EBV-mediated IGF-1 induction
| Project/Area Number |
16590566
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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 | Hokkaido University |
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Principal Investigator |
IWAKIRI Dai Hokkaido University, Institute for genetic medicine, lecturer, 遺伝子病制御研究所, 助手 (10307853)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | EBV / gastric cancer / nasopharyngeal carcinoma / EBER / IGF-1 / RIG-I / 上咽頭癌 / 胃癌 |
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| Research Abstract |
We have previously reported that EBV infection of gastric epithelial cells leads to induction of insulin-like growth factor (IGF)-1 and IGF-1 promotes growth of EBV-infected cells by an autocrine mechanism. We have also identified that EBV-encoded small RNA (EBER) is the responsible gene for IGF-1 induction. In this study, we demonstrated that EBV promotes growth of nasopharyngeal epithelial cells thorough induction of IGF-1 by EBER. Furthermore, we observed high IGF-1 expression in nasopharyngeal carcinoma (NPC) tissues. These findings strongly suggest that EBER plays a significant role in epithelial cancer development. We also tried to assess the mechanism of EBER-mediated IGF-1 induction and identified that EBER induces intracellular signaling through interaction with retinoic acid-inducible gene (RIG)-I (Submitted). Since RIG-I has RNA-helicase domain and Caspase activation and recruiting domain (CARD), it recognizes dsRNA and induces production of interferon and other cytokines through activation of IRF-3 or NF-κB. Our results suggest that EBER-RIG-I interaction induces growth factor expression in EBV-infected cells, and further study is going on.
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Report
(3 results)
Research Products
(7 results)
