Alternative splicing in EMT and TGF-β signaling during cancer progression

被引:10
作者
Zhang, Ying E. [1 ,2 ]
Stuelten, Christina H. [1 ]
机构
[1] NCI, Lab Cellular & Mol Biol, Ctr Canc Res, Bethesda, MD 20892 USA
[2] NIH, Lab Cellular & Mol Biol, Ctr Canc Res, NCI, Bldg 37,RM 2056B, Bethesda, MD 20892 USA
基金
美国国家卫生研究院;
关键词
Alternative splicing; EMT; TGF-beta; splicing factor; PRE-MESSENGER-RNA; TO-MESENCHYMAL TRANSITION; GENOME-WIDE ANALYSIS; REGULATORY NETWORK; DRUG-RESISTANCE; BREAST-CANCER; P120; CATENIN; STEM-CELLS; HNRNP A1; BINDING;
D O I
10.1016/j.semcancer.2024.04.001
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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, cellcell junction changes, cell motility and invasiveness. In advanced cancers, transforming growth factor- beta (TGF- beta ) 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- beta signaling. It will emphasize the importance of various splicing factors involved in EMT and explore their regulatory mechanisms.
引用
收藏
页码:1 / 11
页数:11
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