Toll-like receptor 2 mediates invasion via activating NF-κB in MDA-MB-231 breast cancer cells
Toll-like receptor 2 mediates invasion via activating NF-κB in MDA-MB-231 breast cancer cells
复制标题
DOI：
10.1016/j.bbrc.2009.01.009
复制
发表时间：
2009-02-20
影响因子：
3.1
通讯作者：
Hu, Zhuowei
中科院分区：
文献类型：
--
作者：
Xie, Wenjie;Wang, Yongsheng;Hu, Zhuowei
MDA MB-231 乳腺癌细胞具有很高的侵袭潜力，但所涉及的机制尚不清楚。本研究表明Toll样受体2（TLR2）在MDA-MB-231细胞中高表达，并在细胞侵袭中发挥关键作用。与侵袭性较差的MCF-7细胞相比，MDA-MB-231细胞的TLR2表达量高出10.5倍。使用 TLR2 激动剂 pg-LPS 和 TLR2 中和抗体，我们发现 TLR2 激活显着促进 MDA-MB-231 入侵，而 TLR2 阻断则减弱了这种能力。 TLR2 激活增强了 MDA-MB-231 中 NF-kappa B 的活性，并诱导 TLR2/NF-kappa B 信号通路中 TAK1 和 I kappa B α 的磷酸化，但在 MCF-7 细胞中则不然。 TLR2 激活增加了 IL-6、TGF-β、VEGF 和 MMP9 的分泌，这些分泌与 TLR2-NF-kappa B 信号传导相关。我们证明 TLR2 是负责 NF-KB 信号传导活性和 MDA-MB-231 细胞的高侵袭能力的关键受体。 (C) 2009 Elsevier Inc. 保留所有权利。
MDA MB-231 breast cancer cells have a high invasive potential, yet the mechanisms involved are [lot known. This study showed that Toll-like receptor 2 (TLR2) was highly expressed in MDA-MB-231 cells and played a critical role in cell invasion. Compared with the poorly invasive MCF-7 cells, MDA-MB-231 cells expressed 10.5-fold more TLR2. Using TLR2 agonist pg-LPS and TLR2 neutralizing antibody, We found that TLR2 activation significantly promoted MDA-MB-231 invasion, whereas TLR2 blockade diminished this capacity. TLR2 activation enhanced the activity of NF-kappa B and induced phosphorylation of TAK1 and I kappa B alpha in the TLR2/NF-kappa B signaling pathway in MDA-MB-231, but not in MCF-7 cells. TLR2 activation increased IL-6, TGF-beta, VEGF and MMP9 secretion, which are associated with TLR2-NF-kappa B signalling. We demonstrated that TLR2 is a critical receptor responsible for NF-KB signaling activity and highly invasive capacity of MDA-MB-231 cells. (C) 2009 Elsevier Inc. All rights reserved.