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首页> 外文期刊>Journal of Cellular Physiology >The anti-cancer effects of (-)-epigallocatechin-3-gallate on the signaling pathways associated with membrane receptors in MCF-7 cells.
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The anti-cancer effects of (-)-epigallocatechin-3-gallate on the signaling pathways associated with membrane receptors in MCF-7 cells.

机译：的抗癌作用(-) -epigallocatechin-3-gallate信号途径与膜受体有关MCF-7细胞。

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摘要

(-)-Epigallocatechin-3-gallate (EGCg) has been implicated in cancer chemo-prevention in studies using many different kinds of cancer cells. The present study measured cell viability, osteopontin (OPN) secretion, fatty acid synthase (FAS) expression, and cytosolic Ca(2+) and verified the anti-cancer activities of EGCg in MCF-7 human breast cancer cells. EGCg-induced apoptosis was evidenced by nuclear condensation, increased protein levels of activated caspase-3, down-regulation of gelsolin and tropomyosin-4 (Tm-4), and up-regulation of tropomyosin-1(Tm-1). By disrupting adherens junction formation, EGCg caused accumulation of extra-nuclear beta-catenin aggregates in the cytosol and alterations of the protein content and mRNA expression of E-cadherin and beta-catenin, but not N-cadherin, in MCF-7 cells. To identify the putative mechanisms underlying the EGCg signaling pathways, EGFP (enhanced green fluorescence protein) was ectopically expressed in MCF-7 cells. This allowed us to monitor the EGCg-induced fluorescence changes associated with the effects of Triton X-100 (to remove plasma membrane) or the addition of laminin, anti-laminin receptor (LR) antibody, epidermal growth factor (EGF), and genistein on the cells. Our results indicated that EGCg acts via the signaling pathways associated with cell membrane to suppress cell proliferation, provoke apoptosis, and disturb cell-cell adhesion in MCF-7 cells. The altered events include the EGFR, LR, FAS, intracellular Ca(2+) , OPN secretion, caspace-3, gelsolin, Tm-4, Tm-1, and adherens junction proteins, E-cadherin and beta-catenin.
机译：(-) -Epigallocatechin-3-gallate (EGCg)与癌症化学预防研究使用许多不同类型的癌细胞。本研究测量细胞的生存能力,骨桥蛋白(OPN)分泌脂肪酸合酶(FAS)表达式,胞质Ca(2 +)和验证了EGCg的抗癌活动MCF-7人类乳腺癌细胞。细胞凋亡被核凝结,证明caspase-3激活的蛋白质含量增加,下调gelsolin tropomyosin-4(Tm-4)和老年病的tropomyosin-1 (Tm-1)。通过扰乱adherens结的形成,EGCgextra-nuclearβ-连环蛋白的积累造成的聚集在细胞溶质和改变的蛋白质含量和钙粘蛋白mRNA的表达和β-连环蛋白,但不是N-cadherin MCF-7细胞。EGCg信号通路EGFP的深层次原因(增强型绿色荧光蛋白)ectopically MCF-7表达细胞。允许我们监视EGCg-induced荧光的变化与影响特里同x - 100(去除质膜)或层粘连蛋白,anti-laminin受体(LR)抗体,表皮生长因子(EGF)和染料木素的细胞。通过信号通路,EGCg的行为与细胞膜,抑制细胞有关增殖,引起细胞凋亡和打扰信息在MCF-7细胞粘附。事件包括表皮生长因子受体、LR、FAS,细胞内Ca (2 +), OPN分泌,caspace-3, gelsolin,Tm-4、Tm-1 adherens结蛋白,钙粘蛋白和β-连环蛋白。

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