PMLIV overexpression promotes TGF-β-associated epithelial-mesenchymal transition and migration in MCF-7 cancer cells
Autor: | Jia-Xin Wang, Chun‐Xiao Yu, Xing‐Li Dong, Wan‐Lu Xu, Yu Liu, Xiu-Xian Li, Wei Xia, Dan Zhao, Bing Wang, Wenfeng Chu, Ping Ni, Liang-Liang Li, Di Huang |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Gene isoform Epithelial-Mesenchymal Transition Physiology Clinical Biochemistry Breast Neoplasms Smad2 Protein Biology Promyelocytic Leukemia Protein Models Biological Metastasis 03 medical and health sciences Protein Domains Cell Movement Transforming Growth Factor beta medicine Humans Protein Isoforms Epithelial–mesenchymal transition Smad3 Protein Phosphorylation Cell Nucleus Alternative splicing Cell Biology medicine.disease 030104 developmental biology HEK293 Cells MCF-7 Cancer cell Cancer research MCF-7 Cells Female Signal transduction Transforming growth factor Signal Transduction |
Zdroj: | Journal of cellular physiology. 233(12) |
ISSN: | 1097-4652 |
Popis: | 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 PMLIV 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. |
Databáze: | OpenAIRE |
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