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,1
* Intervention Section, Cell and Cancer Biology Department, Medicine Branch, Division of Clinical Science, National Cancer Institute, and
Head and Neck Surgery Branch, National Institute of Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland 20892, USA; and
Procter and Gamble Oral Health Care Technology Division, Cincinnati, Ohio, USA
2Correspondence: Intervention Section, National Cancer Institute, Bldg. 10/12N226, 9000 Rockville Pike, Bethesda, MD 20892, USA. E-mail: mulshinej{at}bprb.nci.nih.gov
High levels of prostaglandins are produced in human oropharyngeal
carcinoma (OPC). Five human OPC cell lines tested expressed both
isoforms of cyclooxygenases (COX). The pan-COX inhibitor ketorolac
continuously and significantly decreased PGE2 production
and IL-6 and IL-8 levels in all OPC cell lines tested, but did not
affect IL-1
, GM-CSF levels, or in vitro tumor cell
growth. In contrast, ketorolac reduced OPC growth in
vivo. The OPC cell lines used express the IL-6 receptor, and
IL-6 stimulation of these cells causes transduction to occur via STAT3
pathway activation. Coincubation with OPC cell lines with conditioned
medium from a TPA-exposed HL-60 cells stimulated growth proportional to
the IL-6 levels measured in the conditioned medium. This growth effect
was specifically inhibited by anti-IL-6 antibody. These results are
consistent with cytokine products of inflammatory cells having
paracrine growth effects on OPC. If chronic inflammation plays a role
in promoting the development of OPC, this mechanism may also apply to
other epithelial tumor systems modulated by COX activity.—Hong,
S. H., Ondrey, F. G., Avis, I. M., Chen, Z., Loukinova,
E., Cavanaugh, P. F., Jr., Van Waes, C., Mulshine, J. L.
Cyclooxygenase regulates human oropharyngeal carcinomas via the
proinflammatory cytokine IL-6: a general role for inflammation?.
Key Words: colon cancer • arachidonic acid • inflammatory disease • COX inhibitors
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