PMLIV overexpression promotes TGF‐β‐associated epithelial–mesenchymal transition and migration in MCF‐7 cancer cells

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 ident...

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Bibliographic Details
Published in:Journal of cellular physiology 2018-12, Vol.233 (12), p.9575-9583
Main Authors: Liu, Yu, Wang, Jia‐Xin, Huang, Di, Wang, Bing, Li, Liang‐Liang, Li, Xiu‐Xian, Ni, Ping, Dong, Xing‐Li, Xia, Wei, Yu, Chun‐Xiao, Xu, Wan‐Lu, Chu, Wen‐Feng, Zhao, Dan
Format: Article
Language:English
Subjects:
Alternative splicing
Breast cancer
Cancer
epithelial–mesenchymal transition
Growth factors
Isoforms
Leukemia
Mesenchyme
Metastases
Pathogenesis
Phenotypes
Phosphorylation
promyelocytic leukemia
Promyeloid leukemia
Signal transduction
Signaling
Smad2 protein
Splicing
Transforming growth factor
Transforming growth factor-b
transforming growth factor‐β
Translocation
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Summary: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. PMLIV overexpression promotes cancer‐associated epithelial‐mesenchymal transition by activating transforming growth factor‐β signaling, which leads to a more aggressive cancer cell phenotype and increased cell migration.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.26862