Prostagladin E Receptor II and IV Increase the Expression of Martrix Metalloproteinase-7 in PC (Prostate Cancer)-3 Cells.
- Author:
Tae Hyoung KIM
1
;
Young Sun KIM
;
Soon Chul MYOUNG
;
Jun Hyun LEE
;
Eun Ha WON
Author Information
1. Department of Urology, College of Medicine, Chung-Ang University
- Publication Type:Original Article
- Keywords:
Prostate cancer;
Cyclooxygenase;
PGE2 receptor;
Matrilysin
- MeSH:
Basement Membrane;
Carcinogenesis;
Cyclooxygenase 2 Inhibitors;
Disease Progression;
Enzyme-Linked Immunosorbent Assay;
Matrix Metalloproteinase 7;
Neoplasm Metastasis;
Prostaglandin-Endoperoxide Synthases;
Prostate;
Prostatic Neoplasms;
Receptors, Prostaglandin E;
RNA, Messenger;
Tissue Inhibitor of Metalloproteinase-1
- From:Korean Journal of Urology
2004;45(5):478-484
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: The effects of PGE2 receptors (EP1, 2, 3, 4) on the proliferation of prostate cancer cells are still unclear. The degradation of the basement membrane by MMP-2, 7, 9 and TIMP-1, 2 is a critical point in tumor invasion and metastasis. We investigated the effects of PGE2 receptors concerning MMP and TIMP after the treatment of COX-2 inhibitors on prostate cancer cell-lines. MATERIALS AND METHODS: Two prostate cancer cell-lines, PC-3 and DU-145 cells were used in this study. RT-PCR were performed to detect the mRNA expression of EP1, 2, 3, 4, MMP-2, 7, 9 and TIMP-1, 2, MMP-7 was measured by ELISA after being treated with the selective EP2 agonist and EP4 agonist 10(-10), 10(-8), 10(-6) microM respectively. RESULTS: EP2, 3 and 4 mRNA were expressed in both cell-lines. After the NS-398 treatment, EP2 and EP4 mRNA expressions decreased in PC-3 cells. While only the MMP-7 mRNA expression decreased in PC-3 cells after NS-398 treatment, after NS-398 with selective EP2 agonist and EP4 agonist, MMP-7 mRNA expression increased. In PC-3 cells, selective EP2 agonist and EP4 agonist induced a significant dose-dependent increase in MMP-7 production in comparison to the NS-398 treatment group (control) in the conditioned ELISA medium. CONCLUSIONS: These results strongly suggest that COX-2, to some extent, contribute to prostate carcinogenesis at the EP2 and EP4 receptor, which could also be explained by increments of MMP-7 in PC-3 cells. Therefore, these findings show that selective EP inhibitor is useful in preventing specific disease progression in prostate cancer.
