Molecular mechanisms of EDAC (Epithelial Defense Against Cancer)

2017 Fiscal Year Final Research Report

• Project/Area Number: 26250026
• Research Category: Grant-in-Aid for Scientific Research (A)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Tumor biology
• Research Institution: Hokkaido University
• Principal Investigator: Fujita Yasuyuki 北海道大学, 遺伝子病制御研究所, 教授 (50580974)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: 細胞競合

Outline of Final Research Achievements

In this study, we have identified molecules that are involved in EDAC (epithelial defense against cancer) whereby transformed cells are eliminated from epithelia via cell competition with the surrounding normal epithelial cells. First, we have found that expression of a soluble factor ADAMDEC1 is non-cell-autonomously upregulated in normal cells neighboring transformed cells, which positively regulate apical extrusion of transformed cells. In addition, we also demonstrate that expression of COX-2 is increased in normal cells surrounding transformed cells, which induces inflammatory responses thereby negatively regulating cell competition. Collectively, these results indicate the presence of both negative and positive regulators of cell competition.

Free Research Field

分子腫瘍学