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. 2015 Jun 5;2(4):e981443.
doi: 10.4161/23723556.2014.981443. eCollection 2015 Oct-Dec.

The other face of TLR3: A driving force of breast cancer stem cells

Deyong Jia  1 , Lisheng Wang  2
Affiliations

The other face of TLR3: A driving force of breast cancer stem cells

Deyong Jia et al. Mol Cell Oncol. .

Abstract

Activation of TLR3 has long been studied in the field of anticancer immunotherapy. Our recent work revealed that TLR3 also promotes the induction of breast cancer stem cells (CSCs) through co-activation of β-catenin and NF-κB signaling. Targeting these 2 pathways simultaneously instead of individually allows for effective inhibition of CSCs that are enhanced by TLR3 activation.

Keywords: NF-κB; TLR3; breast cancer; cancer stem cells; β-catenin.

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Figures

Figure 1.
Figure 1.
β-catenin signaling is required for breast cancer cells to acquire stem cell features following toll-like receptor 3 (TLR3) activation. Inhibition of both β-catenin and NF-kB is an effective strategy to control the growth of human breast cancer induced by TLR3 activation. c-MYC, NANOG, OCT3/4, and SOX2 are transcriptional factors crucial for the maintenance of pluripotent stem cells and possibly for the induction of CSCs. ALDH1, aldehyde dehydrogenase 1; CSC, cancer stem cell; dsRNA, double-stranded RNA; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; NF-κB p65, nuclear factor NF-kB p65 subunit involved in NF-κB heterodimer formation, nuclear translocation, and activation; Poly(I:C), polyinosinic-polycytidylic acid; TRIF, toll/interleukin-1 receptor-domain-containing adapter-inducing interferon-β.
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