Chibby1 knockdown promotes mesenchymal-to-epithelial transition-like changes
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https://tandf.figshare.com/articles/dataset/Chibby1_knockdown_promotes_mesenchymal-to-epithelial_transition-like_changes/4572706
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Chibby1 (Cby1) was originally isolated as a binding partner for β-catenin, a dual function protein in cell-cell adhesion and in canonical Wnt signaling. The canonical Wnt/β-catenin pathway is dysregulated in various diseases including cancer, most notably of the gastrointestinal origin. To investigate the role of Cby1 in colorectal tumorigenesis, we generated stable Cby1-knockdown (K<sub>D</sub>) SW480 colon cancer cells. Unexpectedly, we found that Cby1 K<sub>D</sub> induces mesenchymal-to-epithelial transition (MET)-like changes in SW480 as well as in HEK293 cells. Cby1-K<sub>D</sub> cells displayed a cuboidal epithelial morphology with tight cell-cell contacts. In Cby1-K<sub>D</sub> cells, the plasma membrane localization of E-cadherin and β-catenin was dramatically increased with formation of cortical actin rings, while the levels of the mesenchymal marker vimentin were decreased. Consistent with these changes, in wound healing assays, Cby1-K<sub>D</sub> cells exhibited epithelial cell-like properties as they migrated collectively as epithelial sheets. Furthermore, the anchorage-independent growth of Cby1-K<sub>D</sub> cells was reduced as determined by soft agar assays. These findings suggest that chronic Cby1 K<sub>D</sub> in colon cancer cells may counteract tumor progression by promoting the MET process.
提供机构：
Taylor & Francis
创建时间：
2017-01-20
