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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Curcumin and Epigallocatechin Gallate Inhibit the Cancer Stem Cell Phenotype via Down-regulation of STAT3-NF kappa B Signaling
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Curcumin and Epigallocatechin Gallate Inhibit the Cancer Stem Cell Phenotype via Down-regulation of STAT3-NF kappa B Signaling

机译：姜黄素和EpigallocateChin Graphate通过Datt3-NF Kappa B信号的下调抑制癌症干细胞表型

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Background/Aim: The cancer stem cell (CSC) model postulates the existence of a small proportion of cancer cells capable of sustaining tumor formation, self-renewal and differentiation. Signal Transducer and Activator of Transcription 3 (STAT3) signaling is known to be selectively activated in breast CSC populations. However, it is yet to be determined which molecular mechanisms regulate STAT3 signaling in CSCs and what chemopreventive agents are effective for suppressing CSC growth. The aim of this study was to examine the potential efficacy of curcumin and epigallocatechin gallate (EGCG) against CSC and to uncover the molecular mechanisms of their anticancer effects. Materials and Methods: To suppress the CSC phenotype, two breast cancer cell lines (MDA-MB-231 cells and MCF7 cells transfected with HER2) were treated with curcumin (10 mu M) with or without EGCG (10 mu M) for 48 h. We used tumor-sphere formation and wound-healing assays to determine CSC phenotype. To quantify CSC populations, Fluorescence-activated cell sorting profiling was monitored. STAT3 phosphorylation and interaction with Nuclear Factor-kB (NFkB) were analyzed by performing western blot and immunoprecipitation assays. Results: Combined curcumin and EGCG treatment reduced the cancer stem-like Cluster of differentiation 44 (CD44)-positive cell population. Western blot and immunoprecipitation analyses revealed that curcumin and EGCG specifically inhibited STAT3 phosphorylation and STAT3-NF kappa B interaction was retained. Conclusion: This study suggests that curcumin and EGCG function as antitumor agents for suppressing breast CSCs. STAT3 and NF kappa B signaling pathways could serve as targets for reducing CSCs leading to novel targeted-therapy for treating breast cancer.
机译：背景/目的：癌症干细胞（CSC）模型消除了能够维持肿瘤形成，自我更新和分化的小比例癌细胞的存在。已知转录3（STAT3）信号传导的信号传感器和活化剂在乳腺CSC群体中选择性地激活。然而，尚不确定哪种分子机制调节CSC中的STAT3信号传导，并且化学预防剂对于抑制CSC生长是有效的。本研究的目的是研究姜黄素和EPIGALLOCATECHIN GALLATE（EGCG）对CSC的潜在疗效，并揭示其抗癌效果的分子机制。材料和方法：为了抑制CSC表型，用姜黄素（10μm）处理两种乳腺癌细胞系（MDA-MB-231细胞和用HER2转染的MCF7细胞），用或没有EGCG（10μm）48小时。我们使用肿瘤球形形成和伤口愈合测定来确定CSC表型。为了量化CSC群体，监测荧光激活的细胞分选分析。通过进行蛋白质印迹和免疫沉淀测定来分析Stat3磷酸化和与核因子-Kb（NFKB）的相互作用。结果：组合姜黄素和EGCG治疗还原癌症干燥的分化簇44（CD44） - 阳性细胞群。蛋白质印迹和免疫沉淀分析显示，保留了姜黄素和EGCG特异性抑制STAT3磷酸化和STAT3-NF kappa B相互作用。结论：该研究表明，姜黄素和EGCG用作抗肿瘤剂用于抑制乳腺CSCs。 STAT3和NF Kappa B信令途径可以作为减少导致新型靶向治疗治疗乳腺癌的CSC的靶标。

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