PMLIV overexpression promotes TGF-β-associated epithelial-mesenchymal transition and migration in MCF-7 cancer cells
PMLIV overexpression promotes TGF-β-associated epithelial-mesenchymal transition and migration in MCF-7 cancer cells
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PMLIV 过表达促进 MCF-7 癌细胞中 TGF-β 相关的上皮间质转化和迁移。
DOI：
10.1002/jcp.26862
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发表时间：
2018-12-01
影响因子：
5.6
通讯作者：
Zhao，Dan
中科院分区：
文献类型：
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作者：
Liu，Yu;Wang，Jia-Xin;Zhao，Dan
上皮-间质转化（EMT）是乳腺肿瘤发生、发展和转移的关键环节。早幼粒细胞白血病（PML）基因通过选择性剪接产生多种异构体，但各异构体的生物学功能尚不清楚。在这项研究中，我们报告了PMLIV（研究最深入的核亚型）在乳腺癌中转化生长因子-β（TGF-β）信号传导相关EMT和迁移中的一个先前未知的作用。这项研究表明，PMLIV过表达促进了更具侵袭性的间充质表型，并增加了MCF-7癌细胞的迁移。该事件与通过诱导Smad 2/3磷酸化和磷酸化Smad 2/3易位至细胞核而激活TGF-β经典信号通路相关。在这项研究中，我们报告了以前未知的作用，PMLIVin TGF-β信号诱导的乳腺癌相关EMT和迁移的调节。靶向该途径可能在治疗上是有益的。
The epithelial–mesenchymal transition (EMT) is a key event associated with metastasis and dissemination in breast tumor pathogenesis. Promyelocytic leukemia (PML) gene produces several isoforms due to alternative splicing; however, the biological function of each specific isoform has yet to be identified. In this study, we report a previously unknown role forPMLIV, the most intensely studied nuclear isoform, in transforming growth factor‐β (TGF‐β) signaling‐associated EMT and migration in breast cancer. This study demonstrates thatPMLIV overexpression promotes a more aggressive mesenchymal phenotype and increases the migration of MCF‐7 cancer cells. This event is associated with activation of the TGF‐β canonical signaling pathway through the induction of Smad2/3 phosphorylation and the translocation of phospho‐Smad2/3 to the nucleus. In this study, we report a previously unknown role forPMLIVin TGF‐β signaling‐induced regulation of breast cancer‐associated EMT and migration. Targeting this pathway may be therapeutically beneficial.