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Proc. Natl. Acad. Sci. USA
Vol. 94, pp. 3336-3340, April 1997
Medical Sciences

Cyclooxygenase-2 expression in human colon cancer cells increases metastatic potential

(invasion / metalloproteinase/prostaglandins/sulindac sulfide)

Masahiko Tsujii*, Sunao Kawano*, and Raymond N. DuBoisdagger

dagger  Departments of Medicine and Cell Biology, Molecular Toxicology Center, Vanderbilt University Medical Center and the Veterans Affairs Medical Center, Nashville, TN 37232; and * First Department of Medicine, Osaka University School of Medicine, Osaka, Japan

Communicated by Philip Needleman, Monsanto Company, St. Louis, MO, January 24, 1997 (received for review September 18, 1996)

Recent epidemiologic studies have shown a 40-50% reduction in mortality from colorectal cancer in individuals who take nonsteroidal antiinflammatory drugs on a regular basis compared with those not taking these agents. One property shared by all of these drugs is their ability to inhibit cyclooxygenase (COX), a key enzyme in the conversion of arachidonic acid to prostaglandins. Two isoforms of COX have been characterized, COX-1 and COX-2. COX-2 is expressed at high levels in intestinal tumors in humans and rodents. Human colon cancer cells (Caco-2) were permanently transfected with a COX-2 expression vector or the identical vector lacking the COX-2 insert. The Caco-2 cells, which constitutively expressed COX-2, acquired increased invasiveness compared with the parental Caco-2 cells or the vector transfected control cells. Biochemical changes associated with this phenotypic change included activation of metalloproteinase-2 and increased RNA levels for the membrane-type metalloproteinase. Increased invasiveness and prostaglandin production were reversed by treatment with sulindac sulfide, a known COX inhibitor. These studies demonstrate that constitutive expression of COX-2 can lead to phenotypic changes that alter the metastatic potential of colorectal cancer cells.


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