Tetraspanin CD63 acts as a pro-metastatic factor via β-catenin stabilization
Ontology highlight
ABSTRACT: The tetraspanin CD63 is implicated in pro-metastatic signaling pathways, but so far, it is unclear how CD63 levels affect the tumor cell phenotype. Here, we investigated the effect of CD63 modulation in different metastatic tumor cell lines. In vitro, knock down of CD63 induced a more epithelial-like phenotype concomitant with increased E-cadherin expression, downregulation of its repressors Slug and Zeb1, and decreased N-cadherin. In addition, β-catenin protein was markedly reduced, negatively affecting expression of the target genes MMP-2 and PAI-1. β-catenin inhibitors mimicked the epithelial phenotype induced by CD63 knock down. Inhibition of β-catenin upstream regulators PI3K/AKT or GSK3β could rescue the mesenchymal phenotype underlining the importance of the β-catenin pathway in CD6
ORGANISM(S): Homo sapiens
SUBMITTER: Kevin Lebrigand
PROVIDER: E-GEOD-61957 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
ACCESS DATA