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首页> 外文期刊>Journal of Cancer >Bleomycin (BLM) Induces Epithelial-to-Mesenchymal Transition in Cultured A549 Cells via the TGF-β/Smad Signaling Pathway
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Bleomycin (BLM) Induces Epithelial-to-Mesenchymal Transition in Cultured A549 Cells via the TGF-β/Smad Signaling Pathway

机译:博来霉素(BLM)通过TGF-β/ Smad信号通路诱导培养的A549细胞上皮向间质转化

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The epithelial-to-mesenchymal transition (EMT) is a crucial cellular event in wound healing, tissue repair, and cancer progression in adult tissues, with the interactions with numerous signals. In this study, we aimed to determine whether bleomycin (BLM), an agent that causes pulmonary fibrosis, induces the EMT of the alveolar epithelial cell line A549 and investigated the possible mechanisms. We examined the EMT involved changes in cell morphology, isoform switching of the fibroblast growth factor receptor 2 (FGFR2) by alternative splicing, and expression of the phenotypic markers including E-cadherin, vimentin, and α-SMA using RT-PCR, Western blotting, and immunofluorescence assays. A TGF-β/Smad inhibitor was used to determine whether coculture with BLM would inhibit the EMT of A549 cells. The results showed that BLM induced the EMT of A549 cells possibly via the TGF-β/Smad signaling pathway, evident from the decrease in the expression of E-cadherin and increase in the expression on vimentin.
机译:上皮-间充质转变(EMT)是成年组织中伤口愈合,组织修复和癌症进展中的关键细胞事件,其相互作用具有多种信号。在这项研究中,我们旨在确定导致肺纤维化的博来霉素(BLM)是否诱导肺泡上皮细胞系A549的EMT,并研究了可能的机制。我们检查了EMT涉及的细胞形态变化,成纤维细胞生长因子受体2(FGFR2)的同种型切换(通过选择性剪接)以及使用RT-PCR,Western印迹的表型标记物(包括E-钙粘蛋白,波形蛋白和α-SMA)的表达和免疫荧光测定。使用TGF-β/ Smad抑制剂来确定与BLM的共培养是否会抑制A549细胞的EMT。结果表明,BLM可能通过TGF-β/ Smad信号传导途径诱导了A549细胞的EMT,这从E-钙黏着蛋白表达的减少和波形蛋白的表达增加可以明显看出。

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