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Tumor Biology |
12,14-prostaglandin J2 Induce Proliferation of Cyclooxygenase-depleted Colorectal Cancer Cells1
Departments of Medicine [R. C., R. J. C., R. G-D., S. C. S., W. E. Z., J. A. O., J. D. M.], Pharmacology [J. A. O., J. D. M.], and Cell Biology [R. C., R. J. C.] and The Vanderbilt Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232; Veterans Administration Medical Center, Nashville, Tennessee 37211 [R. J. C.]; and Department of Histopathology, Imperial College School of Medicine, London W12 OHS, United Kingdom [S. C. K.]
Increased expression of cyclooxygenase (COX) and overproduction of prostaglandins (PGs) have been implicated in the development and progression of colorectal cancer (CRC). Nonsteroidal anti-inflammatory agents (NSAIDS) inhibit growth of various CRC cell lines by both COX-dependent and COX-independent pathways. To specifically examine the effect of COX and PGs on proliferation in CRC cells, we introduced an antisense COX-2 cDNA construct under the control of a tetracycline (Tc)-inducible promoter into a CRC cell line, HCA-7, Colony 29 (HCA-7) that expresses COX and produces PGs. In the presence of Tc, PG production in COX-depleted cells was reduced 99.8% compared with either uninduced transfectants or parental HCA-7 cells. This decrease in PG production was associated with a concomitant 60% reduction in DNA replication. Subsequently, we examined the effects of various PGs to modulate cell growth in COX-depleted HCA-7 or COX-null HCT-15 cells by quantifying [3H]thymidine incorporation and/or growth in collagen gels. We report that J-series cyclopentenone PGs, particularly PGJ2 and 15-deoxy-
12,14-PGJ2, induce proliferation of these cells at nanomolar concentrations. Lipids extracted from parental HCA-7 cell conditioned medium stimulated mitogenesis in COX-depleted HCA-7 cells and COX-null HCT-15 cells. Using chromatographic and mass spectrometric approaches, we were able to detect PGJ2 in conditioned medium from parental HCA-7 cells. Taken together, these findings implicate a role for cyclopentenone PGs in CRC cell proliferation.
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