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Genetic disruption of Ptgs-1, as well as Ptgs-2, reduces intestinal tumorigenesis in Min mice.

Two isoforms of cyclooxygenase (COX) are known, and to date most studies have implicated COX-2, rather than COX-1, as the isoform involved in colon carcinogenesis. In the present study, we show that homologous disruption of either Ptgs-1 or Ptgs-2 (genes coding for COX-1 or COX-2, respectively) reduced polyp formation in Min/+ mice by approximately 80%. Only COX-1 protein was immunohistochemically detected in normal intestinal tissue, whereas both COX-1 and variable levels of COX-2 protein were detected in polyps. Prostaglandin E2 was increased in polyps compared with normal tissue, and both COX-1 and COX-2 contributed to the PGE2 produced. The results indicate that COX-1, as well as COX-2, plays a key role in intestinal tumorigenesis and that COX-1 may also be a chemotherapeutic target for nonsteroidal anti-inflammatory drugs.

Pubmed ID: 10987272

Authors

  • Chulada PC
  • Thompson MB
  • Mahler JF
  • Doyle CM
  • Gaul BW
  • Lee C
  • Tiano HF
  • Morham SG
  • Smithies O
  • Langenbach R

Journal

Cancer research

Publication Data

September 1, 2000

Associated Grants

None

Mesh Terms

  • Animals
  • Crosses, Genetic
  • Cyclooxygenase 1
  • Cyclooxygenase 2
  • Dinoprostone
  • Female
  • Intestinal Neoplasms
  • Intestinal Polyps
  • Intestines
  • Isoenzymes
  • Male
  • Membrane Proteins
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Prostaglandin-Endoperoxide Synthases
  • Reference Values