| First Author | Oh S | Year | 2018 |
| Journal | Cell Signal | Volume | 45 |
| Pages | 102-109 | PubMed ID | 29408223 |
| Mgi Jnum | J:320876 | Mgi Id | MGI:6881157 |
| Doi | 10.1016/j.cellsig.2018.02.003 | Citation | Oh S, et al. (2018) Egr-1 is required for neu/HER2-induced mammary tumors. Cell Signal 45:102-109 |
| abstractText | Egr-1 is known to function mainly as a tumor suppressor through direct regulation of multiple tumor suppressor genes. To determine the role of Egr-1 in breast tumors in vivo, we used mouse models of breast cancer induced by HER2/neu. We compared neu-overexpressing Egr-1 knockout mice (neu/Egr-1 KO) to neu-overexpressing Egr-1 wild type or heterozygote mice (neu/Egr-1 WT or neu/Egr-1 het) with regard to onset of tumor appearance and number of tumors per mouse. In addition, to examine the role of Egr-1 in vitro, we established neu/Egr-1 WT and KO tumor cell lines derived from breast tumors developed in each mouse. Egr-1 deletion delayed tumor development in vivo and decreased the rate of cell growth in vitro. These results suggest that Egr-1 plays an oncogenic role in HER2/neu-driven mammary tumorigenesis. |
