Resistance of prostate cancer cell lines to COX-2 inhibitor treatment

Targeting of cyclooxygenase-2 (COX-2) for cancer chemoprevention is well supported for several tumor types, most notably colon cancer. In contrast, the data for its role in prostate cancer carcinogenesis are correlative only. Thus, we compared the COX-2 expression, activity, and effects of inhibitio...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2005-07, Vol.332 (3), p.800-807
Main Authors: Wagner, Matthew, Loos, James, Weksler, Nicole, Gantner, Marin, Corless, Christopher L., Barry, John M., Beer, Tomasz M., Garzotto, Mark
Format: Article
Language:English
Subjects:
Apoptosis
Apoptosis - drug effects
Cell Line, Tumor
Chemoprevention
Colonic Neoplasms - metabolism
COX-2
Cyclooxygenase 2
Cyclooxygenase 2 Inhibitors
Cyclooxygenase Inhibitors - pharmacology
Dinoprostone - biosynthesis
Drug Resistance, Neoplasm
Humans
Immunohistochemistry
LNCaP
Male
Membrane Proteins
Nitrobenzenes - pharmacology
Prostaglandin E2
Prostaglandin-Endoperoxide Synthases - metabolism
Prostate cancer
Prostatic Neoplasms - drug therapy
Prostatic Neoplasms - enzymology
Prostatic Neoplasms - pathology
Sulfonamides - pharmacology
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Summary:Targeting of cyclooxygenase-2 (COX-2) for cancer chemoprevention is well supported for several tumor types, most notably colon cancer. In contrast, the data for its role in prostate cancer carcinogenesis are correlative only. Thus, we compared the COX-2 expression, activity, and effects of inhibition in prostate cancer cells on COX-2-dependent colon cancer cells. COX-2 levels in benign and malignant human prostate tissue were determined by immunohistochemistry. Compared to colon cancer cells, prostate cancer cells expressed lower levels of COX-2, produced less PGE 2, and were resistant to selective COX-2 inhibition. Examination of benign prostatic epithelium from prostatectomy samples demonstrated rare foci of COX-2. Whereas, human prostate cancer sections were uniformly negative for COX-2. In conclusion, these studies indicate the lack of a putative role for COX-2 in prostate cancer development. Direct evidence for the involvement of COX-2 in prostate cancer carcinogenesis is desperately needed.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2005.05.025