Centre for Cell Chromosome Biology, Biosciences, Centre for Cell and Chromosome Biology, School of Health Sciences and Social Care, Brunel University, Uxbridge, UB8 3PH, UK.
Int J Oncol. 2012 May;40(5):1358-64. doi: 10.3892/ijo.2012.1349. Epub 2012 Jan 27.
Choriocarcinoma is a highly malignant epithelial tumour that is most often associated with hydatidiform mole and presents the most common emergency medical problem in the management of trophoblast disease. We hypothesise that the hormones/cytokines present within the tumour microenvironment play key roles in the development of choriocarcinoma. In this study we assessed the effects of interleukin-1β (IL-1β) on cell death in the presence or absence of the sex hormone progesterone using two choriocarcinoma cell lines (BeWo and JEG-3) as in vitro experimental models. Although IL-1β induced cell death in both cell lines, the effect was more pronounced in JEG-3 cells, where cell death reached 40% compared to 15% in BeWo cells. Cell death of JEG-3 cells in response to IL-1β was significantly decreased by co-treatment with 100 nM and 1000 nM progesterone and completely abolished at a progesterone concentration of 1000 nM. Progesterone was also able to induce phosphorylation of ERK1/2 in these cells. Pretreatment of JEG-3 cells with a specific MAPK inhibitor (UO126) inhibited progesterone's inhibitory effect on cell death. Collectively, these data provide evidence of cross-talk between progesterone and IL-1β in this aggressive and poorly understood tumour that involves activation of a MAPK pathway and involvement of numerous progesterone receptors.
绒癌是一种高度恶性的上皮肿瘤,通常与葡萄胎有关,是滋养层疾病治疗中最常见的紧急医疗问题。我们假设肿瘤微环境中存在的激素/细胞因子在绒癌的发展中起关键作用。在这项研究中,我们使用两种绒癌细胞系(BeWo 和 JEG-3)作为体外实验模型,评估了白细胞介素-1β(IL-1β)在存在或不存在性激素孕酮的情况下对细胞死亡的影响。虽然 IL-1β诱导两种细胞系的细胞死亡,但在 JEG-3 细胞中更为明显,细胞死亡达到 40%,而 BeWo 细胞中为 15%。JEG-3 细胞对 IL-1β的细胞死亡反应通过与 100 nM 和 1000 nM 孕酮共同处理而显著降低,并且在孕酮浓度为 1000 nM 时完全消除。孕酮还能够诱导这些细胞中 ERK1/2 的磷酸化。用特异性 MAPK 抑制剂(UO126)预处理 JEG-3 细胞可抑制孕酮对细胞死亡的抑制作用。总的来说,这些数据提供了证据表明在这种侵袭性和理解甚少的肿瘤中,孕酮和 IL-1β 之间存在相互作用,涉及 MAPK 途径的激活和众多孕酮受体的参与。