Egr-1 is required for neu/HER2-induced mammary tumors

Cell Signal. 2018 May:45:102-109. doi: 10.1016/j.cellsig.2018.02.003. Epub 2018 Feb 2.

Abstract

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.

Keywords: Egr-1; HER2; Mammary tumors; Neu.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / pathology
  • Carcinogenesis / genetics*
  • Cell Proliferation
  • Early Growth Response Protein 1 / genetics
  • Early Growth Response Protein 1 / physiology*
  • Female
  • Gene Deletion
  • Mammary Neoplasms, Experimental / genetics*
  • Mammary Neoplasms, Experimental / pathology
  • Mice, Knockout
  • Receptor, ErbB-2 / metabolism
  • Signal Transduction
  • Tumor Cells, Cultured

Substances

  • Early Growth Response Protein 1
  • Egr1 protein, mouse
  • Erbb2 protein, mouse
  • Receptor, ErbB-2