The Prostaglandin E Receptor Agonists Increase Granulocyte Macrophage Colony-Stimulating Factor in Prostate Cancer Cells.
- Author:
Tae Hyoung KIM
1
;
Young Sun KIM
;
Soon Chul MYUNG
;
Doo Hyung LEE
;
Eun Ha WON
;
Shin Young LEE
Author Information
1. Department of Urology College of Medicine, Chung-Ang University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Prostate cancer;
Cell;
Cyclooxygenase 2;
GM-CSF;
PGE receptor
- MeSH:
Cell Line;
Cell Proliferation;
Cyclooxygenase 2;
Dinoprostone;
Enzyme-Linked Immunosorbent Assay;
Granulocyte-Macrophage Colony-Stimulating Factor;
Granulocytes*;
Macrophage Colony-Stimulating Factor*;
Macrophages*;
Polymerase Chain Reaction;
Prostate*;
Prostatic Neoplasms*;
Receptors, Prostaglandin E*;
Reverse Transcription;
RNA, Messenger
- From:Korean Journal of Urology
2004;45(12):1272-1278
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: The predilection for prostate carcinoma cells to metastasize to bone suggests the hypothesis that bone and/or bone marrow-derived factors may promote prostate carcinoma cell growth and/or their survival. To date, little work has been performed to characterize the nature of granulocyte macrophage colony-stimulating factor (GM-CSF) and the expression of prostaglandin E2 receptors (EPs) in prostate cancer (PC) cells. The aim of this study is to evaluate the effects of GM-CSF on cell proliferation and the effects of EP agonists on the production of GM-CSF in the PC-3 cells. MATERIALS AND METHODS: The bone-derived PC-3 cell line was used in this study. Reverse transcription polymerase chain reaction (RT-PCR) was performed to detect the mRNA expression of EP1, 2, 3 and 4 and hGM- CSF. 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) assay was done to estimate the viability of PC-3 cells after hGM-CSF treatment. hGM-CSF was measured by enzyme-linked immunosorbent assay (ELISA) after treatments with the EPs agonist at 10(-10), 10(-8), 10(-6)M, respectively. RESULTS: EP2, 3 and 4 and hGM-CSF were expressed in the PC-3 cell line. Viability of the PC-3 cells was significantly increased by hGM-CSF administration in a dose- and time-dependent manner. Also, our data indicated that EP2, 3 and especially 4 agonists induced a significant dose- dependent increase in hGM-CSF production in comparison to the control group in the conditioned ELISA medium. CONCLUSIONS: These results suggest that GM-CSF may be part of a network of an autocrine-regulatory loop system that modulates the biologic activity of prostate carcinoma cells. Our data suggest that GM-CSF and EPs may represent a possible novel therapeutic target that manipulates the proliferative rate of prostate tumors.
