上皮-间质转换
癌症研究
MCF-7型
转化生长因子
生物
信号转导
转移
RNA剪接
基因亚型
间充质干细胞
乳腺癌
转化生长因子β
癌细胞
磷酸化
选择性拼接
表型
细胞生物学
癌症
基因
遗传学
核糖核酸
人体乳房
作者
Yu Liu,Jia‐Xin Wang,Di Huang,Bing Wang,Liang‐Liang Li,Xiuxian Li,Ping Ni,Xinxin Dong,Wei Xia,Chenggang Yu,Wan‐Lu Xu,Wenfeng Chu,Daqing Zhao
摘要
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 for PMLIV , the most intensely studied nuclear isoform, in transforming growth factor‐β (TGF‐β) signaling‐associated EMT and migration in breast cancer. This study demonstrates that PMLI V 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 for PMLIV in TGF‐β signaling‐induced regulation of breast cancer‐associated EMT and migration. Targeting this pathway may be therapeutically beneficial.
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