TLR4激动剂和缺氧协同促进人上皮性卵巢癌TLR4/NF-κB/HIF-1α环的形成

Bin Zhao, Xiulong Niu, S. Huang, Jing Yang, Yiying Wei, X. Wang, Junhong Wang, Yue Wang, Xiaoqin Guo
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引用次数: 5

摘要

炎症和缺氧与许多癌症进展有关。据报道,toll样受体4 (TLR4)/核因子κB (NF-κB)通路和缺氧诱导因子1α (HIF-1α)被激活,与上皮性卵巢癌(EOC)的化疗耐药和预后不良密切相关。然而,在EOC中,TLR4/NF-κB和HIF-1α之间的潜在相关性在很大程度上仍然未知。本研究探讨了在EOC组织中TLR4、NF-κB和HIF-1α蛋白之间可能存在的正相关关系。我们的体外实验结果表明,LPS可以通过TLR4/NF-κB信号通路诱导和激活A2780和SKOV3细胞中的HIF-1α。此外,缺氧诱导的TLR4表达和NF-κB下游转录活性依赖于hif -1α。在裸鼠异种移植瘤模型中也证实了TLR4/NF-κB信号通路与HIF-1α之间的串扰。因此,我们首次提出在EOC中形成TLR4/NF-κB/HIF-1α环。正反馈回路增强了炎症和缺氧的易感性和反应性,协同促进了EOC的发生和发展。这种新机制可能作为未来治疗EOC的候选疗法。
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TLR4 Agonist and Hypoxia Synergistically Promote the Formation of TLR4/NF-κB/HIF-1α Loop in Human Epithelial Ovarian Cancer
Inflammation and hypoxia are involved in numerous cancer progressions. Reportedly, the toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) pathway and hypoxia-inducible factor-1α (HIF-1α) are activated and closely related to the chemoresistance and poor prognosis of epithelial ovarian cancer (EOC). However, the potential correlation between TLR4/NF-κB and HIF-1α remains largely unknown in EOC. In our study, the possible positive correlation among TLR4, NF-κB, and HIF-1α proteins was investigated in the EOC tissues. Our in vitro results demonstrated that LPS can induce and activate HIF-1α through the TLR4/NF-κB signaling in A2780 and SKOV3 cells. Moreover, hypoxia-induced TLR4 expression and the downstream transcriptional activity of NF-κB were HIF-1α-dependent. The cross talk between the TLR4/NF-κB signaling pathway and HIF-1α was also confirmed in the nude mice xenograft model. Therefore, we first proposed the formation of a TLR4/NF-κB/HIF-1α loop in EOC. The positive feedback loop enhanced the susceptibility and responsiveness to inflammation and hypoxia, which synergistically promote the initiation and progression of EOC. The novel mechanism may act as a future therapeutic candidate for the treatment of EOC.
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