A novel function of CD82/KAI-1 on E-cadherin-mediated homophilic cellular adhesion of cancer cells.
In this study, we analyzed the effect of the metastasis suppressor CD82/KAI-1, a member of the tetraspanin superfamily, on intercellular adhesion on cancer cells. The newly established invasion assay and the cell aggregation assay revealed that CD82 strengthens E-cadherin-mediated intercellular adhesion. Interestingly, ectopic expression of CD82 stabilized E-cadherin/beta-catenin complex formation. Furthermore, CD82 reduced tyrosine phosphorylation of beta-catenin on HGF stimulation. Taken together, CD82 may stabilize or strengthen E-cadherin-dependent intercellular adhesion by regulating beta-catenin-mediated signal transduction on cancer cells, and consequently, prevent cancer cells from seceding from the primary tumor site.
Abe
Masakazu
M
Department of Oral and Maxillofacial Surgery, Graduate School of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Sugiura
Tsuyoshi
T
Takahashi
Miho
M
Ishii
Kotaro
K
Shimoda
Miyuki
M
Shirasuna
Kanemitsu
K
D015820:Cadherins / Q000378:metabolism*; D002448:Cell Adhesion; D045744:Cell Line, Tumor; D002465:Cell Movement; D006801:Humans; D051861:Kangai-1 Protein / Q000502:physiology*; D009369:Neoplasms / Q000378:metabolism* / Q000473:pathology; D010766:Phosphorylation; D014443:Tyrosine / Q000378:metabolism; D051176:beta Catenin / Q000737:chemistry / Q000378:metabolism
D015820:Cadherins; D051861:Kangai-1 Protein; D051176:beta Catenin; D014443:Tyrosine