James Graham Brown Cancer Center, University of Louisville, KY 40202, USA.
Int J Cancer. 2010 Jan 15;126(2):371-81. doi: 10.1002/ijc.24732.
Rhabdomyosarcoma (RMS) is the most common soft-tissue sarcoma of adolescence and childhood. Because RMS tumors are highly vascularized, we sought to determine which factors secreted by RMS cells are crucial in stimulating angiogenesis in response to hypoxia. To address this issue, we evaluated expression of several proangiogenic factors [interleukin (IL)-8, vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF)-2, stromal-derived factor (SDF)-1, hepatocyte growth factor (HGF) and leukemia inhibitory factor (LIF)] in 8 human RMS cell lines in both normal steady-state and hypoxic conditions. We found by real-time quantitative polymerase chain reaction (RQ-PCR) and confirmed by enzyme-linked immunosorbent assay (ELISA) that from all the factors evaluated, IL-8, whose expression is very low in normoxia, had been very highly expressed and secreted by RMS cells lines during hypoxic conditions ( approximately 40-170 times). Interestingly, this upregulation was not affected by knocking down hypoxia-inducible factor (HIF)-1alpha, but was inhibited by mitogen-activated protein kinase (MAPK)p42/44 and phosphatidylinositaol 3-kinase (PI3K)/AKT pathway inhibitors. This suggests that IL-8 expression is regulated in an activating protein (AP)-1- and nuclear factor (NF)-kappaB-dependent manner. Furthermore, we found that conditioned media (CM) harvested from RMS cells exposed to hypoxia activated and stimulated chemotactic responses in human umbilical vein endothelial cells (HUVECs) and that IL-8 was responsible for hypoxia-related effects. Finally, by employing shRNA, the expression of IL-8 in human RH-30 cells was downregulated. We noticed that such RMS cells, if injected into skeletal muscles of immunodeficient mice, have a reduced ability for tumor formation. We conclude that IL-8 is a pivotal proangiogenic factor released by human RMS cells in hypoxic conditions and that the targeting of IL-8 may prove to be a novel and efficient strategy for inhibiting RMS growth.
横纹肌肉瘤(RMS)是青少年和儿童中最常见的软组织肉瘤。由于 RMS 肿瘤具有高度血管化的特点,我们试图确定 RMS 细胞分泌的哪些因子对于应对缺氧刺激血管生成至关重要。为了解决这个问题,我们在正常稳定状态和缺氧条件下评估了 8 个人 RMS 细胞系中几种促血管生成因子(白细胞介素[IL]-8、血管内皮生长因子[VEGF]、成纤维细胞生长因子[FGF]-2、基质衍生因子[SDF]-1、肝细胞生长因子[HGF]和白血病抑制因子[LIF])的表达。通过实时定量聚合酶链反应(RQ-PCR)发现,并且通过酶联免疫吸附测定(ELISA)证实,在所评估的所有因子中,IL-8 在常氧条件下表达非常低,但在 RMS 细胞系的缺氧条件下高度表达和分泌(约 40-170 倍)。有趣的是,这种上调不受缺氧诱导因子(HIF)-1alpha 的敲低影响,但受丝裂原激活蛋白激酶(MAPK)p42/44 和磷脂酰肌醇 3-激酶(PI3K)/AKT 途径抑制剂的抑制。这表明 IL-8 的表达受到激活蛋白(AP)-1 和核因子(NF)-kappaB 依赖性调节。此外,我们发现缺氧暴露的 RMS 细胞产生的条件培养基(CM)激活并刺激人脐静脉内皮细胞(HUVEC)的趋化反应,并且 IL-8 是与缺氧相关的效应的原因。最后,通过使用 shRNA 下调 RH-30 细胞中 IL-8 的表达。我们注意到,如果将此类 RMS 细胞注射到免疫缺陷小鼠的骨骼肌中,其肿瘤形成能力降低。我们得出结论,IL-8 是人类 RMS 细胞在缺氧条件下释放的关键促血管生成因子,针对 IL-8 可能被证明是抑制 RMS 生长的一种新颖有效的策略。