Transgenic expression of cyclooxygenase-2 in mouse intestine epithelium is insufficient to initiate tumorigenesis but promotes tumor progression

Cancer Lett. 2009 Jan 18;273(2):225-32. doi: 10.1016/j.canlet.2008.08.012. Epub 2008 Sep 14.


We generated mice expressing a COX-2 transgene in colon epithelium and found that they did not develop spontaneous colon tumors. But when treated with azoxymethane, a colon carcinogen, COX-2 mice had a higher tumor load compared to wild-type mice. There was no change in the number of pre-neoplastic lesions, indicating that COX-2 does not affect tumor initiation. Tumors in the COX-2 transgenic mice had higher levels of phosphorylated epidermal growth factor receptor and Akt compared to wild-type mice. Collectively, our data indicate that COX-2 promotes colon tumor progression, but not initiation, and it does so, in part, by activating EGFR and Akt signaling pathways.

Publication types

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

MeSH terms

  • Animals
  • Cyclooxygenase 2 / biosynthesis
  • Cyclooxygenase 2 / genetics*
  • Disease Progression
  • Epithelium / metabolism*
  • ErbB Receptors / metabolism*
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Intestinal Mucosa / metabolism*
  • Male
  • Mice
  • Mice, Transgenic
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction
  • Transgenes*


  • Cyclooxygenase 2
  • ErbB Receptors
  • Proto-Oncogene Proteins c-akt