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首页> 外文期刊>Cancer Cell International >C-phycocyanin inhibits epithelial-to-mesenchymal transition in Caski cells
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C-phycocyanin inhibits epithelial-to-mesenchymal transition in Caski cells

机译:C-植物植物蛋白抑制Caski细胞上皮对间充质转变

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In cervical cancer, most patients die of metastasis. The epithelial-to-mesenchymal transition (EMT) is a pivotal and intricate process that increases the metastatic potential of cervical cancer. C-phycocyanin (C-PC) is a natural marine product isolated and purified from Spirulina platensis, has been investigated that has anti-cancer function. The aim of this study was to explore the inhibitory effect of C-phycocyanin on the migration and invasion of cervical cancer cells induced by transforming growth factor-β1 (TGF-β1), so as to provide a new idea for the treatment and prognosis of cervical cancer. A wound-healing assay, an invasion assay, immunofluorescence assay, western blot, flow cytometry and real-time reverse transcriptione polymerase chain reaction were explored in cervical cancer Caski cell lines. TGF-β/smad signaling pathway was evaluated of in Caski cell lines. Our study indicated that TGF-β1 induced EMT in cervical cancer cells. C-phycocyanin inhibited EMT in Caski cells by down-regulating N-cadherin and up-regulating E-cadherin protein expression. Furthermore, C-phycocyanin could inhibit the expression and proteins Twist, Snail and Zeb1 transcription factors related to EMT. In addition, C-phycocyanin could inhibit the migration and invasion of Caski cells induced by TGF-β1. Besides, C-phycocyanin inhibited EMT through TGF-β/smads signaling pathway. We also found C-phycocyanin induced cell cycle G0/G1 arrest by decreasing protein expression levels of Cyclin D1 and p27. C-phycocyanin reversed TGF-β1-induced epithelial-to-mesenchymal transition in cervical cancer cells and down-regulated the TGF-β/samd signaling pathway induced G0/G1 arrest of tumor cell cycle.
机译:在宫颈癌中,大多数患者死于转移。上皮 - 间充质转换(EMT)是枢轴和复杂的方法,增加宫颈癌的转移性潜力。 C-植物植物(C-PC)是从螺旋藻液体分离并纯化的天然船舶产品,已经研究具有抗癌功能。本研究的目的是探讨C-植物苷素对通过转化生长因子-β1(TGF-β1)诱导的宫颈癌细胞迁移和侵袭的抑制作用,以便为治疗和预后提供新的思路宫颈癌。在宫颈癌Caski细胞系中探讨了伤口愈合测定,侵袭测定,免疫荧光测定,蛋白质印迹,流式细胞术和实时逆转录聚合酶链反应。在Caski细胞系中评估TGF-β/ Smad信号通路。我们的研究表明,TGF-β1在宫颈癌细胞中诱导EMT。通过下钙蛋白和上钙蛋白和Up-Cathherin蛋白表达,C-植物植物抑制Caski细胞的EMT。此外,C-植酸胞苷可以抑制与EMT相关的表达和蛋白质扭曲,蜗牛和Zeb1转录因子。此外,C-植酸胞苷可以抑制TGF-β1诱导的Caski细胞的迁移和侵袭。此外,C-植物植物蛋白通过TGF-β/ Smads信号通路抑制EMT。我们还通过降低细胞周期蛋白D1和P27的蛋白质表达水平,发现C-植物植物诱导细胞周期G0 / G1滞留。 C-植物植物在宫颈癌细胞中逆转TGF-β1诱导的上皮 - 间充质转变,下调TGF-β/ SAMD信号通路诱导肿瘤细胞周期的G0 / G1停滞。

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