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姜黄素通过抑制 NF-κB-Snail 信号通路抑制 LPS 诱导的 EMT 进程在乳腺癌细胞中。

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

机构信息

Department of Orthopedic Surgery, Affiliated Hospital of Xi'an Medical College, Xi'an 710077, PR China.

出版信息

Oncol Rep. 2013 Jan;29(1):117-24. doi: 10.3892/or.2012.2080. Epub 2012 Oct 16.

Abstract

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-κB-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-κB-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.

摘要

上皮-间充质转化 (EMT) 被认为是癌细胞侵袭和转移的关键事件。新出现的证据表明,姜黄素可能预防或延迟癌症的进展,其作用部分可能是由于其破坏 EMT 的能力,但尚未得到证实。在这项研究中,我们使用脂多糖 (LPS) 触发 MCF-7 和 MDA-MB-231 乳腺癌细胞系中的 EMT,并表明姜黄素抑制 LPS 诱导的形态变化,降低 LPS 诱导的 EMT 标志物如波形蛋白的表达,并增加 E-钙粘蛋白的表达,从而抑制体外细胞迁移和侵袭。我们发现这些作用是通过 NF-κB-Snail 信号通路的失活介导的。我们的结果表明,姜黄素通过下调 NF-κB-Snail 活性,在抑制 LPS 诱导的乳腺癌细胞 EMT 中发挥重要作用。这些数据为姜黄素的抗侵袭机制提供了新的视角,表明其作用部分归因于其攻击 EMT 过程的能力。

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