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.

已知Egr-1主要通过直接调节多个肿瘤抑制基因而主要起肿瘤抑制作用。为了确定Egr-1在体内乳腺肿瘤中的作用，我们使用了由HER2 / neu诱导的乳腺癌小鼠模型。我们比较了neu高表达的Egr-1基因敲除小鼠（neu / Egr-1 KO）与neu高表达的Egr-1野生型或杂合子小鼠（neu / Egr-1 WT或neu / Egr-1 het）的发病机理肿瘤外观和每只小鼠的肿瘤数量。另外，为了检查Egr-1在体外的作用，我们建立了neu / Egr-1 WT和KO肿瘤细胞系，这些细胞系源自于每只小鼠体内发育的乳腺肿瘤。Egr-1缺失可延缓体内肿瘤的发展，并降低体外细胞的生长速度。这些结果表明，Egr-1在HER2 / neu驱动的乳腺肿瘤发生中起着致癌作用。