Epithelial-to-mesenchymal transition (EMT) is a process in which epithelial cells lose their junctions and polarity to gain a motile mesenchymal phenotype. EMT is essential during embryogenesis and adult physiological processes like wound healing, but is aberrantly activated in pathological conditions like fibrosis and cancer. A series of transcription factors (EMT-inducing transcription factor; EMT-TF) regulate the induction of EMT by repressing the transcription of epithelial genes while activating mesenchymal genes through mechanisms still debated. The nuclear interaction of EMT-TFs with larger protein complexes involved in epigenetic genome modulation has attracted recent attention to explain functions of EMT-TFs during reprogramming and cellular differentiation. In this review, we discuss recent advances in understanding the interplay between epigenetic regulators and EMT transcription factors and how these findings could be used to establish new therapeutic approaches to tackle EMT-related diseases.

上皮-间充质转变（EMT）是一个过程，其中上皮细胞失去连接和极性，从而获得活动的间充质表型。EMT在胚胎发生和成年生理过程（如伤口愈合）过程中至关重要，但在诸如纤维化和癌症的病理情况下会异常激活。一系列转录因子（EMT诱导转录因子； EMT-TF）通过抑制上皮基因的转录，同时通过尚有争议的机制激活间充质基因来调节EMT的诱导。EMT-TFs与参与表观遗传基因组调控的较大蛋白复合物的核相互作用最近引起人们的关注，以解释EMT-TFs在重编程和细胞分化过程中的功能。在这篇评论中，