Curcumin inhibits LPS-induced EMT through downregulation of NF-κB-Snail signaling in breast cancer cells

被引:127
作者
Huang, Tao [2 ]
Chen, Zhijun [2 ]
Fang, Liping [1 ]
机构
[1] Jinling Hosp Nanjing, Dept Resp Med, Nanjing 210001, Jiangsu, Peoples R China
[2] Xian Med Coll, Affiliated Hosp, Dept Orthoped Surg, Xian 710077, Peoples R China
关键词
curcumin; breast cancer; NF-kappa B; invasion; epithelial-mesenchymal transition; EPITHELIAL-MESENCHYMAL TRANSITION; CHEMOPREVENTIVE AGENTS; CLINICAL-TRIALS; E-CADHERIN; EXPRESSION; PROGRESSION; INVASION; METASTASIS; MECHANISM; PATHWAY;
D O I
10.3892/or.2012.2080
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Epithelial-mesenchymal transition (EMT) is considered a critical event in cancer cell invasion and metastasis. Emerging evidence has shown that curcumin may prevent or delay the progression of cancer, an effect that may be partially due to its ability to disrupt EMT, yet this has not yet been demonstrated. In this study, we used lipopolysaccharide (LPS) to trigger EMT in MCF-7 and MDA-MB-231 breast cancer cell lines and showed that curcumin inhibited LPS-induced morphological changes, decreased the expression of LPS-induced markers of EMT such as vimentin, and increased the expression of E-cadherin, resulting in the inhibition of in vitro cell motility and invasiveness. We discovered that these actions were mediated through the inactivation of NF-kappa B-Snail signaling pathways. Our results indicate that curcumin plays an important role in the inhibition of LPS-induced EMT in breast cancer cells through the downregulation of NF-kappa B-Snail activity. These data provide a new perspective of the anti-invasive mechanism of curcumin, indicating that the effect is partly due to its ability to attack the EMT process.
引用
收藏
页码:117 / 124
页数:8
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