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C-藻蓝蛋白抑制转化生长因子-β1诱导的人上皮细胞上皮-间质转化。

C-phycocyanin suppresses transforming growth factor-β1-induced epithelial mesenchymal transition in human epithelial cells.

作者信息

Pattarayan Dhamotharan, Rajarajan Dheeran, Ayyanar Sivanantham, Palanichamy Rajaguru, Subbiah Rajasekaran

机构信息

Department of Biotechnology, Anna University, BIT-Campus, Tiruchirappalli, Tamil Nadu, India.

Department of Biotechnology, Anna University, BIT-Campus, Tiruchirappalli, Tamil Nadu, India.

出版信息

Pharmacol Rep. 2017 Jun;69(3):426-431. doi: 10.1016/j.pharep.2016.12.013. Epub 2017 Jan 5.

DOI:10.1016/j.pharep.2016.12.013
PMID:28288400
Abstract

BACKGROUND

Epithelial mesenchymal transition (EMT) is a process through which epithelial cells undergo multiple biochemical changes, causing them to differentiate into a mesenchymal-cell phenotype. This process has been shown to contribute to the development of fibrotic diseases. C-phycocyanin (C-PC) is a phycobiliprotein extracted from Spirulina platensis. This study was done to investigate the effect of C-PC on transforming growth factor-β1 (TGF-β1)-induced EMT and an EMT associated proliferation in human epithelial cell lines.

METHODS

Human adenocarcinoma cell line, A549 and breast cancer cell line, MCF-7 were treated with TGF-β1, and EMT-related genes expression, cell proliferation and cell cycle arrest were examined.

RESULTS

C-PC suppressed the EMT as assessed by reduced expression of vimentin, type-1-collagen and fibronectin, and increased E-cadherin expression in TGF-β1 treated cells. Further, TGF-β1 treatment induced cell cycle arrest in S and G2/M phase in A549 cells. However, TGF-β1-mediated cell cycle arrest was significantly reversed by combined treatment with C-PC.

CONCLUSIONS

The overall data suggested that C-PC suppresses TGF- β1-induced EMT and warrants further in vivo studies for future evaluation of C-PC as a potential antifibrotic agent.

摘要

背景

上皮-间质转化(EMT)是上皮细胞经历多种生化变化,使其分化为间充质细胞表型的过程。已证明该过程有助于纤维化疾病的发展。C-藻蓝蛋白(C-PC)是从钝顶螺旋藻中提取的一种藻胆蛋白。本研究旨在探讨C-PC对转化生长因子-β1(TGF-β1)诱导的人上皮细胞系EMT及EMT相关增殖的影响。

方法

用人腺癌细胞系A549和乳腺癌细胞系MCF-7进行TGF-β1处理,并检测EMT相关基因表达、细胞增殖和细胞周期阻滞情况。

结果

通过检测波形蛋白、I型胶原蛋白和纤连蛋白的表达降低以及TGF-β1处理细胞中E-钙黏蛋白表达增加来评估,C-PC抑制了EMT。此外,TGF-β1处理诱导A549细胞在S期和G2/M期发生细胞周期阻滞。然而,C-PC联合处理显著逆转了TGF-β1介导的细胞周期阻滞。

结论

总体数据表明,C-PC抑制TGF-β1诱导的EMT,值得进一步进行体内研究,以便将来评估C-PC作为一种潜在抗纤维化药物的作用。

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