Elevated cyclooxygenase-2 levels in Min mouse adenomas.
BACKGROUND & AIMS: Mutations in the APC gene result in an increased propensity to develop intestinal neoplasia; however, a complete understanding of the mechanisms resulting in tumor formation has remained elusive. Min mice possess a mutation in the APC gene and display a neoplastic phenotype similar to that observed in familial adenomatous polyposis coli in humans. Cyclooxygenase ( COX) inhibitors decrease tumor multiplicity in the Min mouse intestine. The present study was designed to determine if there was an increase in COX-2 in adenomas harvested from Min mouse intestine. METHODS: COX-2 messenger RNA levels were determined by Northern blots and reverse-transcription polymerase chain reactions of B6Min x 129 mouse-derived tumors. Protein levels and localization were determined by Western blots and immunohistochemical staining. RESULTS: The Northern blots revealed an approximately threefold increase in the level of COX-2 messenger RNA in Min mouse adenoma compared with normal mucosa. COX-2 protein levels in adenomatous tissues were also approximately threefold higher compared with normal mucosa from the same mouse. Immunohistochemical staining with a monospecific COX-2 antibody confirmed that increases in COX-2 immunoreactivity were restricted to dysplastic and neoplastic foci within intestinal mucosa. CONCLUSIONS: These data show that COX-2 levels may be increased at an early stage in colorectal neoplasia during polyp formation and before invasion.[1]References
- Elevated cyclooxygenase-2 levels in Min mouse adenomas. Williams, C.S., Luongo, C., Radhika, A., Zhang, T., Lamps, L.W., Nanney, L.B., Beauchamp, R.D., DuBois, R.N. Gastroenterology (1996) [Pubmed]
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