2012 Fiscal Year Final Research Report

The role of Afadin in tumorigenesis and tumor progression

Research Project

Project/Area Number	23701071
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Tumor biology
Research Institution	Research Institute, Osaka Medical Center for Cancer and Cardiovascular Disaeses
Principal Investigator	OKAMOTO Miki 地方独立行政法人大阪府立病院機構大阪府立成人病センター(研究所), 研究所, 研究員 (20332455)
Project Period (FY)	2011 – 2012
Keywords	細胞接着 / 運動 / 発がん / 腸上皮細胞
Research Abstract	Afadin interacts with the cytoplasmic region of nectins, immunoglobulin-like cell adhesion molecules at adherens junctions, links them to the actin cytoskeleton, and regulates cytoskeletal remodeling. However, it remains unknown whether afadin plays roles in tumorigenesis and tumor progression. Previously we reported that in afadin intestine-specific deficient mice, the paracellular permeability in the intestinal mucosa increased and susceptibility to the tissue destruction induced by dextran sulfate sodium enhanced. Here we treated the mice with azoxymethan and dextran sulfate sodium, and analyzed the incidence of colitis-associated colon cancer. Mice conditionally lacking afadin in the intestines showed significantly increased the incidence of colon cancer. These results indicate the uppressive role of afadin in developing colitis-associated colon cancer in mice.