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近日，國(guó)際生物學(xué)期刊cell death &differentiation發(fā)表了來(lái)自加拿大和中國(guó)科學(xué)家的一項(xiàng)最近研究成果。研究人員通過(guò)體內(nèi)和體外實(shí)驗(yàn)證明激活toll-like receptor 3(TLR3)能夠促進(jìn)乳腺癌細(xì)胞向腫瘤干細(xì)胞(CSC)轉(zhuǎn)化，產(chǎn)生干細(xì)胞特征，而TLR3的這種促CSC轉(zhuǎn)化效應(yīng)需要同時(shí)激活β catenin和NF-κB信號(hào)通路才能發(fā)生。這一研究成果為癌癥治療中抑制CSC產(chǎn)生提供了新的策略。

研究人員指出，在2012年的統(tǒng)計(jì)中，乳腺癌是導(dǎo)致女性死亡的第二大疾病。傳統(tǒng)療法如放療和化療能夠消除腫瘤腫塊，但對(duì)少數(shù)具有惡性作用的腫瘤細(xì)胞仍然不能起到完全殺死的作用，這些惡性腫瘤細(xì)胞仍然能夠存活并自我更新，進(jìn)一步發(fā)展為惡性腫瘤，這一類細(xì)胞就叫做腫瘤干細(xì)胞。研究發(fā)現(xiàn)，腫瘤干細(xì)胞對(duì)傳統(tǒng)療法具有抵抗作用，并且能夠在某些條件下由非腫瘤干細(xì)胞轉(zhuǎn)化而來(lái)。而TLR3在不良預(yù)后的乳腺癌病人中具有更高的表達(dá)，但TLR3與乳腺癌細(xì)胞向腫瘤干細(xì)胞轉(zhuǎn)化之間的關(guān)系仍然不清楚。

研究人員首先通過(guò)體外細(xì)胞培養(yǎng)發(fā)現(xiàn)，激活TLR3能夠促進(jìn)乳腺癌細(xì)胞產(chǎn)生類似腫瘤干細(xì)胞的特征，但TLR5,7,8并不能起到相同作用。通過(guò)對(duì)機(jī)制進(jìn)一步探討，單獨(dú)激活NF-κB信號(hào)通路并不能引起乳腺癌細(xì)胞向腫瘤干細(xì)胞的轉(zhuǎn)化，而當(dāng)同時(shí)激活β catenin和NF-κB信號(hào)同路時(shí)，才能夠促進(jìn)TLR3介導(dǎo)的乳腺癌細(xì)胞向腫瘤干細(xì)胞的轉(zhuǎn)化。研究人員還發(fā)現(xiàn)，利用小豆蔻明處理乳腺癌細(xì)胞能夠阻斷β catenin和NF-κB信號(hào)通路，導(dǎo)致TLR3介導(dǎo)的CSC轉(zhuǎn)化過(guò)程受到抑制。

綜上所述，該項(xiàng)研究發(fā)現(xiàn)TLR3能夠同時(shí)激活β catenin和NF-κB信號(hào)通路，促進(jìn)乳腺癌細(xì)胞向腫瘤干細(xì)胞轉(zhuǎn)化，并且發(fā)現(xiàn)小豆蔻明能夠阻斷TLR3的這種作用，抑制腫瘤細(xì)胞向腫瘤干細(xì)胞的轉(zhuǎn)化。這一研究成果為抑制CSC產(chǎn)生，提高癌癥治愈率提供了新的策略。

原文標(biāo)題：β -Catenin and NF-κB co-activation triggered by TLR3 stimulation facilitates stem Cell-like phenotypes in breast cancer

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.

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