Korean J Urol.
2001 Oct;42(10):1101-1107.
Effects of Cyclooxygenase-2 on Prostatic Cancer Cell Lines
- Affiliations
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- 1Department of Urology, Chung-Ang University College of Medicine, Seoul, Korea. caucih@dreamwiz.com
Abstract
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PURPOSE: Cyclooxygenases (COXs) are key enzymes in the conversion of arachidonic acid to prostaglandins and other ecosanoids. There are two isoforms of COX, a constitutive one is COX-1 and inducible counterpart is COX-2. COX-2 promotes colorectal tumorigenesis, metastatic potential and angiogenesis. COX-2 inhibitors induce apoptotic cell death and prostaglandin E2 induces its expression. For examination of the action mechanism of COX-2, we investigated expression of bcl-2 related genes through the treatment of COX-2 selective inhibitor, NS-398 on two prostatic cancer cell lines.
MATERIALS AND METHODS
Two prostatic cancer cell lines, PC-3 and LNCaP, were used. MTT assay was done to estimate the viability of prostatic cancer cells after NS-398 treatment. COX-2, bcl-2, bcl-XL, mcl-1, bfl-1, bax, bak, bik and bcl-Xs mRNA expression levels were evaluated by RT-PCR and cDNA Southern blot.
RESULTS
The viability of PC-3 and LNCaP cells were decreased by NS-398 treatment. COX-2 mRNA expression was confirmed in PC-3 and LNCaP cells but faintly expressed in LNCaP cells. Bcl-2, bcl-XL, mcl-1, bfl-1, bax, bak, bik and bcl-Xs mRNA were expressed in both cell lines. After NS-398 treatment, bax-alpha mRNA expression were increased and bfl-1 was decreased in PC-3 cells.
CONCLUSIONS
COX-2 inhibitor, NS-398 decreases the viability of PC-3 and LNCaP cells. Its mechanism is probably partially related with bfl-1 and bax-alpha mRNA expression levels. Because NS-398 induced apoptotic cell death can be develped by COX-2 protein independent pathway, additional experiment is needed by COX-2 transfection method.