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Korean Journal of Urology ; : 786-790, 2006.
Article in Korean | WPRIM | ID: wpr-212191

ABSTRACT

PURPOSE: Interleukin-6 (IL-6) can stimulate a variety of tumors including prostatic carcinoma. Research has recently shown that IL-6 may act to stimulate the progression of prostatic cancer. IL-6 is elevated in the sera of patients with metastatic prostatic cancer and it has been shown to be a candidate marker of disease activity. To date, little work has been performed to characterize the nature of granulocyte macrophage colony-stimulating factor (GM-CSF) and the expression of IL-6. The aim of this study is to evaluate the effects of GM-CSF on the expression of IL-6 in 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 GM-CSF and also the IL-6 mRNA expression. The IL-6 protein was measured by enzyme-linked immunosorbent assay (ELISA) after treatments with the hGM-CSF. RESULTS: hGM-CSF was expressed in the PC-3 cell line. Our data indicated that the IL-6 mRNA expression was not increased at 4, 8 and 12 hours by the hGM-CSF in comparison to the control group, but it was slightly increased at 24 and 48 hours. The expression of IL-6 protein was increased at 4, 8, 12, 24 and 48 hours after hGM-CSF treatment, in comparison with the control group. CONCLUSIONS: The IL-6 mRNA expression was slightly increased by hGM-CSF at 24 and 48 hours in comparison to the control group. Yet the IL-6 protein expression increased before the IL-6 mRNA expression. Therefore, hGM-CSF may modulate the post-transcription pathway of the IL-6 expression in prostate carcinoma cells. Our data suggest that GM-CSF may have a possible IL-6 mediated pathophysiologic role in prostate cancer.


Subject(s)
Humans , Cell Line , Enzyme-Linked Immunosorbent Assay , Granulocyte-Macrophage Colony-Stimulating Factor , Granulocytes , Interleukin-6 , Macrophage Colony-Stimulating Factor , Macrophages , Polymerase Chain Reaction , Prostate , Prostatic Neoplasms , Reverse Transcription , RNA, Messenger
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