Transgenic expression of cyclooxygenase-2 in mouse intestine epithelium is insufficient to initiate tumorigenesis but promotes tumor progression
Copyright policy )Transgenic expression of cyclooxygenase-2 in mouse intestine epithelium is insufficient to initiate tumorigenesis but promotes tumor progression
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.
- University of Utah United States
- Center for Molecular Medicine and Immunology United States
- University of Utah Health Care United States
- University of Connecticut Health Center United States
- Huntsman Cancer Institute United States
Male, Mice, Transgenic, Epithelium, ErbB Receptors, Gene Expression Regulation, Neoplastic, Mice, Cyclooxygenase 2, Disease Progression, Animals, Humans, Female, Transgenes, Intestinal Mucosa, Proto-Oncogene Proteins c-akt, Signal Transduction
Male, Mice, Transgenic, Epithelium, ErbB Receptors, Gene Expression Regulation, Neoplastic, Mice, Cyclooxygenase 2, Disease Progression, Animals, Humans, Female, Transgenes, Intestinal Mucosa, Proto-Oncogene Proteins c-akt, Signal Transduction
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).31 popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.Average influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).Top 10% impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.Top 10%
Citations provided by BIP!Popularity provided by BIP!