Mechanisms of EBV-mediated gastric carcinogenesis through the exosome-induced signaling.

2016 Fiscal Year Final Research Report

• Project/Area Number: 26460932
• Research Category: Grant-in-Aid for Scientific Research (C)
• 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
• Keywords: EBウイルス / 胃がん / EBER / TLR3

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.

Free Research Field

医歯薬学