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首页> 外文期刊>Journal of Pharmacy and Pharmaceutical Sciences >Inhibition of TLR4/TRIF/IRF3 Signaling Pathway by Curcumin in Breast Cancer Cells
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Inhibition of TLR4/TRIF/IRF3 Signaling Pathway by Curcumin in Breast Cancer Cells

机译：抑制TLR4 / TRIF / IRF3信号传导途径在乳腺癌细胞中的姜黄素

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Purpose: Toll-like receptor 4 (TLR4) is over-expressed in breast tumors and thus contributing to the tumor progression and metastasis. Natural products have drawn attention in cancer immunotherapy due to their various biological activities. Curcumin is well investigated in different types of cancer. However, the mechanisms underlying its anti-inflammatory actions have not been extensively elucidated.? For this purpose, we explored the inhibitory effects of curcumin on lipopolysaccharide (LPS)-induced TLR4 dependent TRIF signaling pathway in two subtypes of breast cancer cell lines (MCF-7 and MDA-MB-231) in this study. Methods: In this context, the cytotoxicity of curcumin and LPS alone and the combination of curcumin with LPS on these cells was evaluated by WST-1 assay.? The expression level of TLR4 and the release of type I interferon (IFN) levels were determined after treatment with curcumin and/or LPS by RT-PCR and ELISA analysis, respectively. Furthermore, the subcellular localization of TLR4 and interferon regulatory factor 3 (IRF3) were detected by immunofluorescence analysis. Results: Curcumin treatment suppressed breast cancer cells viabilities and the activation of TLR4-mediated TRIF signaling pathway by the downregulation of TLR4 and IRF3 expression levels and the inhibition of type I IFN (IFN-α/β) levels induced by LPS. However, curcumin was more efficient in MDA-MB-231 cells than MCF-7 cells owing to its greater inhibitory efficacy in the LPS- enhanced TLR4 signaling pathway. Furthermore, IFN-α/β levels induced by TLR4 and IRF3 were decreased in these cells following curcumin treatment. Conclusions: Consequently, these results demonstrated that the activation of LPS stimulated TLR4/TRIF/IRF3 signaling pathway was mediated by curcumin in breast cancer cells, in vitro. However, more studies are necessary to examine the curcumin’s anti-inflammatory activities on TLR4/MyD88/NF-κB as well as other signaling pathways downstream of TLRs in breast cancer.
机译：目的：在乳腺肿瘤中过度表达Toll样受体4（TLR4），从而有助于肿瘤进展和转移。由于其各种生物活动，天然产品引起了癌症免疫疗法。姜黄素在不同类型的癌症中得到很好的研究。然而，其抗炎作用的潜在机制尚未得到广泛阐明。为此目的，我们探讨了吡菌蛋白对脂多糖（LPS）的抑制作用 - 在该研究中的两种乳腺癌细胞系（MCF-7和MB-231）中的两种亚型中的TLR4依赖性TrIF信号传导途径。方法：在这种情况下，通过WST-1测定评估这些细胞上单独的姜黄素和LPS的细胞毒性和姜黄素与LPS的组合。在用RT-PCR和ELISA分析分别在用姜黄素和/或LPS处理后测定TLR4的表达水平和I型干扰素（IFN）水平。此外，通过免疫荧光分析检测TLR4和干扰素调节因子3（IRF3）的亚细胞定位。结果：姜黄素处理抑制乳腺癌细胞的活力和TLR4介导的TRIF信号传导途径的激活通过TLR4和IRF3表达水平的下调和LPS诱导的I型IFN（IFN-α/β）水平的抑制。然而，由于其LPS-增强的TLR4信号通路中的抑制效力，姜黄素在MDA-MB-231细胞中比MDA-MB-231细胞更有效。此外，在姜黄素处理后，通过TLR4和IRF3诱导的IFN-α/β水平在这些细胞中降低。结论：因此，这些结果表明，LPS刺激的TLR4 / TRIF / IRF3信号传导途径的激活是通过姜黄素在乳腺癌细胞中介导的，体外介导。然而，更多的研究是在乳腺癌中检查TLR4 / MyD88 / NF-κB上的姜黄素的抗炎活性以及在TLR下游的其他信号通路。

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