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首页> 美国卫生研究院文献>Cell Death and Differentiation >β-Catenin and NF-κB co-activation triggered by TLR3 stimulation facilitates stem cell-like phenotypes in breast cancer
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β-Catenin and NF-κB co-activation triggered by TLR3 stimulation facilitates stem cell-like phenotypes in breast cancer

机译：TLR3刺激触发的β-Catenin和NF-κB共激活促进乳腺癌干细胞样表型

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Cancer stem cells (CSCs) are responsible for tumor initiation and progression. Toll-like receptors (TLRs) are highly expressed in cancer cells and associated with poor prognosis. However, a linkage between CSCs and TLRs is unclear, and potential intervention strategies to prevent TLR stimulation-induced CSC formation and underlying mechanisms are lacking. Here, we demonstrate that stimulation of toll-like receptor 3 (TLR3) promotes breast cancer cells toward a CSC phenotype in vitro and in vivo. Importantly, conventional NF-κB signaling pathway is not exclusively responsible for TLR3 activation-enriched CSCs. Intriguingly, simultaneous activation of both β-catenin and NF-κB signaling pathways, but neither alone, is required for the enhanced CSC phenotypes. We have further identified a small molecule cardamonin that can concurrently inhibit β-catenin and NF-κB signals. Cardamonin is capable of effectively abolishing TLR3 activation-enhanced CSC phenotypes in vitro and successfully controlling TLR3 stimulation-induced tumor growth in human breast cancer xenografts. These findings may provide a foundation for developing new strategies to prevent the induction of CSCs during cancer therapies.
机译：癌症干细胞（CSC）负责肿瘤的发生和发展。 Toll样受体（TLR）在癌细胞中高度表达，并与不良预后相关。但是，CSC和TLR之间的联系尚不清楚，并且缺乏防止TLR刺激引起的CSC形成和潜在机制的潜在干预策略。在这里，我们证明了在体外和体内刺激Toll样受体3（TLR3）促进乳腺癌细胞向CSC表型发展。重要的是，常规的NF-κB信号通路并不专门负责富含TLR3激活的CSC。有趣的是，增强CSC表型需要同时激活β-catenin和NF-κB信号通路，但不能单独激活。我们进一步鉴定了可以同时抑制β-catenin和NF-κB信号的小分子豆蔻素。小豆蔻素能够在体外有效地消除TLR3激活增强的CSC表型，并成功地控制TLR3刺激诱导的人乳腺癌异种移植物中的肿瘤生长。这些发现可能为开发新的策略以防止在癌症治疗过程中诱导CSCs提供基础。

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