Mechanisms of EBV-mediated gastric carcinogenesis through the exosome-induced signaling.
Project/Area Number |
26460932
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | University of Human Arts and Sciences (2016) Kobe University (2015) Hokkaido University (2014) |
Principal Investigator |
Iwakiri Dai 人間総合科学大学, 人間科学部, 特任教授 (10307853)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | EBウイルス / 胃がん / EBER / TLR3 / EBV / エクソソーム / 自然免疫 |
Outline of Final Research Achievements |
We demonstrated that EBV-encoded small RNA (EBER) is released by EBV-infected gastric cancer (GC) cells through the exosome secretion and exosomal transfer of EBER triggers the signaling from toll-like receptor 3 in the recipient cells. EBER-mediated activation of TLR3 signals led to the growth promotion of EBV-infected gastric cancer cells, suggesting that exosomal transfer of EBER contributes to gastric carcinogenesis. Further study revealed that treatment with exosome inhibitor reduces the growth potential of EBV-infected GC cells.
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Report
(4 results)
Research Products
(10 results)