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*
Department of Oncological Sciences, Huntsman Cancer Institute, Salt Lake City, UT 84108; and
Department of Pharmacology, University of Colorado Health Sciences Center, Denver, CO 80262
Induction of genes encoding cytokines or other, unidentified
proteins may contribute to the pharmacological effects of taxol. We
hypothesized that prostaglandin H synthase-2 (PGHS-2) was one of the
unidentified genes induced by taxol. Taxol alone or taxol plus IFN-
increased PGE2 formation, PGHS-2 protein expression, and
PGHS-2 mRNA expression in RAW 264.7 murine macrophages. The kinetics
for mRNA induction, protein expression, and catalysis were
self-consistent. A selective inhibitor of PGHS-2 blocked
PGE2 formation by cells incubated with taxol; a selective
inhibitor of PGHS-1 had no effect. A glucocorticoid blocked the
induction of mRNA, the expression of PGHS-2 protein, and the formation
of PGE2. Neither taxol alone nor taxol plus IFN- altered
the expression of the PGHS-1 isoenzyme in RAW 264.7 cells. Taxotere, an
analogue that stabilizes microtubules as potently as taxol, did not
alter the expression of PGHS-2, implying that its induction in RAW
264.7 murine macrophages did not originate from microtubule
stabilization. Taxol and taxotere each induced PGHS-2 expression in
human monocytes suspended in 10% human serum. However, human monocytes
suspended in 10% bovine serum responded only to LPS, not to taxol or
taxotere, implying that they act independently of the LPS-mimetic
process that is prominent in mice. Taxol induced PGHS-2 in human and
murine monocytes via a p38 mitogen-associated protein kinase pathway.
The inclusion of PGHS-2 among the early response genes induced in
leukocytes may be relevant to the beneficial and adverse effects
encountered during taxol administration.
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