Epithelial-mesenchymal transition (EMT) is recognized as a driving force of cancer cell metastasis and drug resistance, two leading causes of cancer recurrence and cancer-related death. It is, therefore, logical in cancer therapy to target the EMT switch to prevent such cancer metastasis and recurrence. Previous reports have indicated that growth factors (such as epidermal growth factor and fibroblast growth factor) and cytokines (such as the transforming growth factor beta (TGF-β) family) are major stimulators of EMT. However, the mechanisms underlying EMT initiation and progression remain unclear. Recently, emerging evidence has suggested that reactive oxygen species (ROS), important cellular secondary messengers involved in diverse biological events in cancer cells, play essential roles in the EMT process in cancer cells by regulating extracellular matrix (ECM) remodeling, cytoskeleton remodeling, cell-cell junctions, and cell mobility. Thus, targeting EMT by manipulating the intracellular redox status may hold promise for cancer therapy. Herein, we will address recent advances in redox biology involved in the EMT process in cancer cells, which will contribute to the development of novel therapeutic strategies by targeting redox-regulated EMT for cancer treatment.

中文翻译：

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肿瘤细胞上皮-间质转化中的氧化还原调节：分子基础和治疗策略。

上皮-间质转化（EMT）被认为是癌细胞转移和耐药性的驱动力，这是癌症复发和癌症相关死亡的两个主要原因。因此，在癌症治疗中，以EMT开关为靶点以预防此类癌症转移和复发是合乎逻辑的。先前的报道表明，生长因子（例如表皮生长因子和成纤维细胞生长因子）和细胞因子（例如转化生长因子β（TGF-β）家族）是EMT的主要刺激因子。但是，EMT启动和发展的潜在机制仍不清楚。最近，越来越多的证据表明，活性氧（ROS）是参与癌细胞中各种生物学事件的重要细胞次级信使，通过调节细胞外基质（ECM）重塑，细胞骨架重塑，细胞间连接和细胞迁移，在癌细胞的EMT过程中发挥重要作用。因此，通过操纵细胞内的氧化还原状态靶向EMT可能为癌症治疗带来希望。在本文中，我们将探讨癌细胞中EMT过程所涉及的氧化还原生物学的最新进展，这些进展将通过靶向氧化还原调节的EMT进行癌症治疗，从而有助于开发新的治疗策略。