| First Author | Miura Y | Year | 2014 |
| Journal | Exp Cell Res | Volume | 327 |
| Issue | 1 | Pages | 146-55 |
| PubMed ID | 24881817 | Mgi Jnum | J:217574 |
| Mgi Id | MGI:5614550 | Doi | 10.1016/j.yexcr.2014.05.019 |
| Citation | Miura Y, et al. (2014) CCAAT/enhancer binding protein beta (C/EBPbeta) isoform balance as a regulator of epithelial-mesenchymal transition in mouse mammary epithelial cells. Exp Cell Res 327(1):146-55 |
| abstractText | Activation of the epithelial-mesenchymal transition (EMT) program promotes cell invasion and metastasis, and is reversed through mesenchymal-epithelial transition (MET) after formation of distant metastases. Here, we show that an imbalance of gene products encoded by the transcriptional factor C/EBPbeta, LAP (liver-enriched activating protein) and LIP (liver-enriched inhibitory protein), can regulate both EMT- and MET-like phenotypic changes in mouse mammary epithelial cells. By using tetracycline repressive LIP expression constructs, we found that SCp2 cells, a clonal epithelial line of COMMA1-D cells, expressed EMT markers, lost the ability to undergo alveolar-like morphogenesis in 3D Matrigel, and acquired properties of benign adenoma cells. Conversely, we found that inducible expression of LAP in SCg6 cells, a clonal fibroblastic line of COMMA1-D cells, began to express epithelial keratins with suppression of proliferation. The overexpression of the C/EBPbeta gene products in these COMMA1-D derivatives was suppressed by long-term cultivation on tissue culture plastic, but gene expression was maintained in cells grown on Matrigel or exposed to proteasome inhibitors. Thus, imbalances of C/EBPbeta gene products in mouse mammary epithelial cells, which are affected by contact with basement membrane, are defined as a potential regulator of metastatic potential. |
