上皮细胞可塑性、上皮-间充质转化和 TGF-β 家族。

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

机构信息

Department of Molecular Pathology, Graduate School of Medicine, the University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.

Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, and Department of Cell and Tissue Biology, University of California at San Francisco, San Francisco, CA 94143, USA.

出版信息

Dev Cell. 2021 Mar 22;56(6):726-746. doi: 10.1016/j.devcel.2021.02.028.

DOI:10.1016/j.devcel.2021.02.028

PMID:33756119

Abstract

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-β and TGF-β-related proteins playing prominent instructive roles. Epithelial-mesenchymal transitions (EMTs) directed by activin-like molecules, bone morphogenetic proteins, or TGF-β 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-β and TGF-β-related proteins, and underlying molecular mechanisms, in epithelial plasticity in development and wound healing, fibrosis, and cancer.

摘要

上皮细胞抑制上皮特征，并表现出间充质特征，以迁移到其他位置并获得新的特性。上皮细胞可塑性反应是通过信号通路的合作来指导的，其中 TGF-β 和 TGF-β 相关蛋白起着突出的指导作用。由激活素样分子、骨形态发生蛋白或 TGF-β 指导的上皮-间充质转化 (EMT) 调节后生动物的发育和伤口愈合，并推动纤维化和癌症的进展。在癌中，不同的 EMT 使干细胞生成、抗癌药物耐药性、基因组不稳定性和局部免疫抑制成为可能。这篇综述讨论了 TGF-β 和 TGF-β 相关蛋白在发育和伤口愈合、纤维化和癌症中的上皮可塑性中的作用和潜在的分子机制。