Interleukin-1beta가 전립선암세포 PC-3 및 DU-145의 증식력과 Interleukin-6 및 Interleukin-6 수용체 mRNA 발현에 미치는 영향Interleukin-1beta Modulates Proliferation, Interleukin-6 and Interleukin Receptor Expression in PC-3 and DU-145 Prostatic Cancer Cells
- Authors
- 명순철; 안승용; 오승영; 원은하; 박언섭; 김경도
- Issue Date
- 2004
- Publisher
- 대한비뇨기과학회
- Keywords
- Prostatic cancer; Cell; Interleukin-1beta; IL-6; IL-6 receptor
- Citation
- Investigative and Clinical Urology, v.45, no.8, pp 810 - 816
- Pages
- 7
- Journal Title
- Investigative and Clinical Urology
- Volume
- 45
- Number
- 8
- Start Page
- 810
- End Page
- 816
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/28633
- ISSN
- 2466-0493
2466-054X
- Abstract
- Purpose: IL-1 is a multifunctional proinflammatory cytokine. As the proliferative effects of IL-6 and IL-6 receptor expressions on prostatic cancer cells in response to IL-1 have not been determined, the effects of IL-1 on prostatic cancer cell lines were investigated.
Materials and Methods: PC-3 and DU-145 cells were cultured in RPMI-1640 medium containing 10% fetal bovine serum. Cell cultures were supplemented with various concentrations of IL-1(0, 1, 10, 20 and 40ng/ ml), and the MMT growth assay performed. PC-3 and DU-145 cells were treated for 2, 4, 8, 12 and 24 h both with and without IL-1. IL-6 and IL-6 receptor(IL-6R) mRNA expressions were investigated using RT-PCR, and the IL-6 levels in cultured supernatant measured by ELISA.
Results: The viability of both PC-3 and DU-145 cells decreased after IL-1 treatment(10, 20 and 40ng/ml). With 40ng/ml the IL-1, IL-6 and IL-6RmRNA expressions were lower in PC-3 cells, but unchanged in DU-145 cells, whereas the IL-6 protein production was higher in both PC-3 and DU-145 cells.
Conclusions: IL-1 inhibited the proliferation of both PC-3 and DU145 cells. In the PC-3 cells, IL-1 decreased the expressions of IL-6 and IL-6R mRNA, but paradoxically increased the IL-6 production. In the DU-145 cells, IL-1 treatment did not affect the IL-6 or IL-6R mRNA expressions, but the IL-6 production was increased. This discrepancy between IL-1-induced IL-6 mRNA and protein production may be mediated by modification to the protein synthesis or an increased cellular excretion. (Korean J Urol 2004; 45:810-816)
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