Downregulation of -catenin decreases the tumorigenicity, but promotes epithelial-mesenchymal transition in breast cancer cells

Background: Wnt/-catenin signaling pathway plays a key role in human breast cancer progression. In this study, we down regulated -catenin expression in human breast cancer MDA-MB-231 cells and investigated the effect of -catenin knockdown on the cell biological characteristics. Materials and Methods: The recombinant plasmids of pSUPER-enhancement green fluorescent protein 1 (EGFP1)-scrabble--catenin-short hairpin ribonucleic acid (shRNA) and pSUPER-EGFP1--catenin-shRNA-1 were transfected into MDA-MB-231 cells, respectively, and the stably transfected cells were isolated from G418 selected clones. The -catenin gene silenced efficiency was measured by quantitative reverse transcriptase polymerase chain reaction (QRT-PCR) and Western blot. The biological characteristics of MDA-MB-231 cells with down regulated -catenin were evaluated by analyzing cell proliferation, clonogenicity, cell mobility and tumorigenicity. The expression of E-cadherin and Vimentin was concurrently detected by QRT-PCR. Results: The -catenin-shRNA-1 stably transfected MDA-MB-231 cells significantly decreased -catenin expression, cell proliferation, clonogenicity, and tumorigenicity in Balb/c nude mice compared with the MDA-MB-231 cells transfected with pSUPER-EGFP1-scrabble--catenin-shRNA. Interestingly, knockdown of -catenin led to the reduction of epithelial E-cadherin expression, the increase of cell mobility and mesenchymal vimentin expression in MDA-MB-231 cells, indicating an epithelial to mesenchymal transition. Conclusion: Knockdown of -catenin expression in human breast cancer MDA-MB-231 cells inhibits cell tumorigenicity in mice, but promotes cell epithelial-mesenchymal transition.