전립선암세포주 PC-3에서 Prostaglandin E 수용체 촉진제에 의한 Granulocyte Macrophage Colony-Stimulating Factor의 증가

초록

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, 10-6M, 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. (Korean J Urol 2004;45:1272-1278)

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