Epithelial-mesenchymal transition (EMT) has been linked with aggressive tumor biology and therapy resistance. It plays central role not only in the generation of cancer stem cells (CSCs) but also direct them across the multiple organ systems to promote tumor recurrence and metastasis. CSCs are reported to express stem cell genes as well as specific cell surface markers and allow aberrant differentiation of progenies. It facilitates cancer cells to leave primary tumor, acquire migratory characteristics, grow into new environment and develop radio-chemo-resistance. Based on the current information, present review discusses and summarizes the recent advancements on the molecular mechanisms that derive epithelial plasticity and its major role in generating a subset of tumor cells with stemness properties and pathophysiological spread of tumor. This paper further highlights the critical need to examine the regulation of EMT and CSC pathways in identifying the novel probable therapeutic targets. These improved therapeutic strategies based on the co-administration of inhibitors of EMT, CSCs as well as differentiated tumor cells may provide improved anti-neoplastic response with no tumor relapse.

中文翻译：

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上皮可塑性和癌症干细胞：癌症发病机理和治疗抗性的主要机制。

上皮-间质转化（EMT）与侵袭性肿瘤生物学和治疗耐药性有关。它不仅在癌症干细胞（CSC）的产生中起着核心作用，而且还指导它们跨多个器官系统促进肿瘤的复发和转移。据报道，CSCs表达干细胞基因以及特定的细胞表面标记，并允许后代异常分化。它促进癌细胞离开原发性肿瘤，获得迁徙特征，成长为新环境并发展放射化学抗性。基于目前的信息，本综述讨论并总结了分子生物学机制的最新进展，这些分子机制产生上皮可塑性及其在产生具有干性和肿瘤病理生理学特征的肿瘤细胞亚群中的主要作用。本文进一步强调了在确定新的可能的治疗靶标时检查EMT和CSC途径的调节的迫切需要。这些基于EMT，CSCs和分化的肿瘤细胞抑制剂共同给药的改良治疗策略可提供改善的抗肿瘤反应，而无肿瘤复发。