| 陈海滔,徐 超,姚庆华.姜黄素通过调节Wnt/β-catenin信号通路抑制结肠癌细胞上皮间质转化[J].肿瘤学杂志,2017,23(1):35-39. |
| 姜黄素通过调节Wnt/β-catenin信号通路抑制结肠癌细胞上皮间质转化 |
| Curcumin Inhibits Tumor Epithelial-Mesenchymal Transition by Downregulating Wnt/β-Catenin Signaling Pathway in Colon Cancer |
| 投稿时间：2016-10-10 |
| DOI：10.11735/j.issn.1671-170X.2017.01.B007 |
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| 中文关键词: 姜黄素 Wnt/β-catenin信号通路 上皮间质转化 |
| 英文关键词:curcumin Wnt/β-catenin signaling pathway epithelial-mesenchymal transition |
| 基金项目:国家自然科学基金（81673813） |
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| 摘要点击次数: 2098 |
| 全文下载次数: 846 |
| 中文摘要: |
| 摘 要：［目的］ 探讨姜黄素对结肠癌细胞上皮间质转化（EMT）的作用机制。 ［方法］ 通过MTS检测姜黄素对HCT116细胞活性的影响；运用Western- blot、Real-time qPCR检测不同浓度姜黄素对HCT116细胞Wnt相关基因（β-catenin、TCF4）及EMT相关基因（E-cadherin和Vimentin）的表达情况。［结果］ 姜黄素能明显抑制HCT116细胞的增殖活性，在12h、24h和48h的IC50分别是61.98±2.68μmol/L，19.64±1.29μmol/L和17.84±1.25μmol/L。姜黄素能下调HCT116细胞内β-catenin和TCF4的表达水平；同时显著性上调E-cadherin及下调Vimentin表达水平，且呈剂量依赖性。Wnt信号通路活化剂能上调姜黄素处理后细胞内的β-catenin表达和下调E-cadherin表达水平。［结论］ 姜黄素通过抑制Wnt/β-catenin信号通路，从而抑制肿瘤细胞上皮间质转化。 |
| 英文摘要: |
| Abstract：［Objective］ To investigate the mechanism of curcumin on epithelial-mesenchymal transition (EMT) of colon cancer cells. ［Methods］ The effects of curcumin on the activity of HCT116 cells were detected by MTS. The expression of Wnt-related genes(β-catenin and TCF4) and EMT-related genes (E-cadherin and Vimentin) were detected by Western-blot and real-time qPCR assay in HCT116 cells. ［Results］ Curcumin could significantly inhibit the proliferation of HCT116 cells and the IC50 at 12h、24h and 48h respectively were 61.98±2.68μmol/L，19.64±1.29μmol/L and 17.84±1.25μmol/L respectively. Curcumin could also down-regulate the expression of β-catenin and TCF4 in HCT116 cells. At the same time，curcumin could up-regulate the expression of E-cadherin and down-regulate the expression of Vimentin in a dose-dependent manner in HCT116 cells. After treatment with Wnt signaling pathway activator，the expression of β-catenin increased and the expression of E-cadherin decresed in HCT116 cells treated with curcumin. ［Conclusion］ Curcumin can inhibit the epithelial-mesenchymal transition by inhibiting the Wnt/β-catenin signaling pathway in tumor cells. |
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