Santarosa Manuela, Maestro Roberta
Unit of Oncogenetics and Functional Oncogenomics, CRO Aviano, National Cancer Institute, IRCCS, 33081 Aviano, Italy.
Cancers (Basel). 2021 Dec 16;13(24):6328. doi: 10.3390/cancers13246328.
Cell-to-cell adhesion is a key element in epithelial tissue integrity and homeostasis during embryogenesis, response to damage, and differentiation. Loss of cell adhesion and gain of mesenchymal features, a phenomenon known as epithelial to mesenchymal transition (EMT), are essential steps in cancer progression. Interestingly, downregulation or degradation by endocytosis of epithelial adhesion molecules (e.g., E-cadherin) associates with EMT and promotes cell migration. Autophagy is a physiological intracellular degradation and recycling process. In cancer, it is thought to exert a tumor suppressive role in the early phases of cell transformation but, once cells have gained a fully transformed phenotype, autophagy may fuel malignant progression by promoting EMT and conferring drug resistance. In this review, we discuss the crosstalk between autophagy, EMT, and turnover of epithelial cell adhesion molecules, with particular attention to E-cadherin.
细胞间黏附是胚胎发育、损伤应答和分化过程中上皮组织完整性和稳态的关键要素。细胞黏附丧失和间充质特征获得，即上皮-间充质转化（EMT）现象，是癌症进展的关键步骤。有趣的是，上皮黏附分子（如E-钙黏蛋白）通过内吞作用下调或降解与EMT相关，并促进细胞迁移。自噬是一种生理性细胞内降解和再循环过程。在癌症中，它被认为在细胞转化的早期阶段发挥肿瘤抑制作用，但一旦细胞获得完全转化的表型，自噬可能通过促进EMT和赋予耐药性来推动恶性进展。在本综述中，我们讨论自噬、EMT和上皮细胞黏附分子周转之间的相互作用，尤其关注E-钙黏蛋白。
