Epithelial plasticity, epithelial-mesenchymal transition, and the TGF-β family

被引：136
作者：
Katsuno, Yoko [1 ]
Derynck, Rik [2 ,3 ]
机构：
[1] Univ Tokyo, Grad Sch Med, Dept Mol Pathol, Bunkyo Ku, Tokyo 1130033, Japan
[2] Univ Calif San Francisco, Eli & Edythe Broad Ctr Regenerat Med & Stem Cell, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Dept Cell & Tissue Biol, San Francisco, CA 94143 USA
来源：
DEVELOPMENTAL CELL | 2021年 / 56卷 / 06期
关键词：
GROWTH-FACTOR-BETA; NEURAL CREST CELLS; CANCER STEM-CELLS; E-CADHERIN; MIR-200; FAMILY; MASTER REGULATOR; IN-VIVO; TRANSFORMING GROWTH-FACTOR-BETA-1; TARGETED DISRUPTION; GENOMIC INSTABILITY;
D O I：
10.1016/j.devcel.2021.02.028
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Epithelial cells repress epithelial characteristics and elaborate mesenchymal characteristics to migrate to other locations and acquire new properties. Epithelial plasticity responses are directed through cooperation of signaling pathways, with TGF-beta and TGF-beta-related proteins playing prominent instructive roles. Epithelial-mesenchymal transitions (EMTs) directed by activin-like molecules, bone morphogenetic proteins, or TGF-beta regulate metazoan development and wound healing and drive fibrosis and cancer progression. In carcinomas, diverse EMTs enable stem cell generation, anti-cancer drug resistance, genomic instability, and localized immunosuppression. This review discusses roles of TGF-beta and TGF-beta-related proteins, and underlying molecular mechanisms, in epithelial plasticity in development and wound healing, fibrosis, and cancer.
引用
收藏
页码：726 / 746
页数：21
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