癌细胞通过可塑性适应不同的应激条件以求生存。干细胞表现出高度的可塑性，使它们能够产生更多的干细胞或将它们分化为特定的细胞类型，以促进组织发育、生长和修复。癌细胞也可以表现出可塑性，并获得增强其生存能力的性质。TGF-β 是癌细胞利用的无与伦比的生长因子，以获得可塑性。TGF-β介导的信号传导使癌症细胞能够通过上皮间质可塑性（EMP）改变它们的上皮和间质特性。然而，TGF-β 是一种多功能细胞因子，因此，TGF-β 的信号传导对癌细胞的影响在细胞上下文中可能有害或有益。那些克服了TGF-β 的抗肿瘤效应的细胞可以诱导上皮间质转变（EMT），以获得 EMP 的益处。EMP 使癌细胞能够改变其细胞性质和肿瘤免疫微环境（TIME），从而促进其生存。由于 TGF-β 和 EMP 在癌瘤进展中的重要作用，了解 TGF-β 如何实现 EMP 以及癌细胞如何利用这种可塑性至关重要。这一认识将指导有效的针对 TGF-β 的治疗方法的开发，以消除癌细胞的可塑性。版权所有©2023。由Elsevier Ltd.出版。

Cancer cells adapt to varying stress conditions to survive through plasticity. Stem cells exhibit a high degree of plasticity, allowing them to generate more stem cells or differentiate them into specialized cell types to contribute to tissue development, growth, and repair. Cancer cells can also exhibit plasticity and acquire properties that enhance their survival. TGF-β is an unrivaled growth factor exploited by cancer cells to gain plasticity. TGF-β-mediated signaling enables carcinoma cells to alter their epithelial and mesenchymal properties through epithelial-mesenchymal plasticity (EMP). However, TGF-β is a multifunctional cytokine; thus, the signaling by TGF-β can be detrimental or beneficial to cancer cells depending on the cellular context. Those cells that overcome the anti-tumor effect of TGF-β can induce epithelial-mesenchymal transition (EMT) to gain EMP benefits. EMP allows cancer cells to alter their cell properties and the tumor immune microenvironment (TIME), facilitating their survival. Due to the significant roles of TGF-β and EMP in carcinoma progression, it is essential to understand how TGF-β enables EMP and how cancer cells exploit this plasticity. This understanding will guide the development of effective TGF-β-targeting therapies that eliminate cancer cell plasticity.Copyright © 2023. Published by Elsevier Ltd.