Interleukin-1beta and fibroblast growth factor receptor 1 cooperate to induce cyclooxygenase-2 during early mammary tumourigenesis

Breast Cancer Res. 2009;11(2):R21. doi: 10.1186/bcr2246. Epub 2009 Apr 24.

Abstract

Introduction: Inflammation within the tumour microenvironment correlates with increased invasiveness and poor prognosis in many types of cancer, including breast cancer. We have previously demonstrated that activation of a mouse mammary tumour virus (MMTV)-driven inducible fibroblast growth factor receptor 1 (iFGFR1) transgene in mammary epithelial cells results in an inflammatory response characterised by induction of inflammatory genes in the mammary gland. Specifically, we have observed increased levels of IL-1beta expression in the mammary gland following activation of iFGFR1 and have used the iFGFR1 model to elucidate the function of IL-1beta in promoting iFGFR1-induced mammary lesions.

Methods: To determine the functional consequences of IL-1beta induction during FGFR1-induced mammary tumourigenesis, the effects of IL-1beta inhibition on the formation of epithelial hyperplasias were examined using the MMTV-iFGFR1 transgenic mouse model. Further studies used a combination of the HC-11 mammary epithelial cell line that stably expresses iFGFR1 and the MMTV-iFGFR1 transgenic mice to further define the mechanisms of IL-1beta function.

Results: Inhibition of IL-1beta activity in vivo resulted in reduced iFGFR1-induced epithelial proliferation and formation of hyperplastic structures. Further studies demonstrated that treatment of mammary epithelial cells with IL-1beta-induced expression of cyclooxygenase (Cox)-2 both in vitro and in vivo. Finally, inhibition of Cox-2 prior to activation of iFGFR1 in the transgenic mice also resulted in decreased iFGFR1-induced formation of hyperplastic structures.

Conclusions: The results from these studies indicate that targeting the inflammatory cytokine IL-1beta partially inhibits iFGFR1-induced formation of early-stage mammary lesions, in part through induction of Cox-2. These findings demonstrate that activation of a growth factor receptor in mammary epithelial cells results in increased expression of inflammatory mediators, which cooperate to promote the initiation of hyperplastic lesions in the mammary gland.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Western
  • Cell Movement
  • Cyclooxygenase 2 / biosynthesis*
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Hyperplasia
  • Immunoenzyme Techniques
  • Interleukin-1beta / physiology*
  • Mammary Neoplasms, Experimental / enzymology*
  • Mammary Neoplasms, Experimental / pathology
  • Mice
  • Mice, Transgenic
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Phenotype
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Receptor, Fibroblast Growth Factor, Type 1 / physiology*
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • Interleukin-1beta
  • NF-kappa B
  • RNA, Messenger
  • Ptgs2 protein, mouse
  • Cyclooxygenase 2
  • Fgfr1 protein, mouse
  • Receptor, Fibroblast Growth Factor, Type 1