Epithelial to mesenchymal transition (EMT) is a physiological process during development where epithelial cells transform to acquire mesenchymal characteristics, which allows them to migrate and colonize secondary tissues. Many cellular signaling pathways and master transcriptional factors exert a myriad of controls to fine tune this vital process to meet various developmental and physiological needs. Adding to the complexity of this network are post-transcriptional and post-translational regulations. Among them, alternative splicing has been shown to play important roles to drive EMT-associated phenotypic changes, including actin cytoskeleton remodeling, cell-cell junction changes, cell motility and invasiveness. In advanced cancers, transforming growth factor-β (TGF-β) is a major inducer of EMT and is associated with tumor cell metastasis, cancer stem cell self-renewal, and drug resistance. This review aims to provide an overview of recent discoveries regarding alternative splicing events and the involvement of splicing factors in the EMT and TGF-β signaling. It will emphasize the importance of various splicing factors involved in EMT and explore their regulatory mechanisms.
Keyphrases
- epithelial mesenchymal transition
- transforming growth factor
- single cell
- cell therapy
- signaling pathway
- gene expression
- transcription factor
- stem cells
- bone marrow
- squamous cell carcinoma
- air pollution
- mesenchymal stem cells
- cell proliferation
- pseudomonas aeruginosa
- cystic fibrosis
- cell migration
- lymph node metastasis
- biofilm formation
- network analysis