Epithelial-to-mesenchymal transition (EMT) initiates malignant transformation of cancer cells and is responsible for the generation of heterogenic subsets of cancer stem cells (CSCs). Signals in the form of environmental cues and paracrine factors within tumor microenvironment (TME) niche, support the possibility of generation of pool of CSCs with two distinct functional transition states. Cyclic CSCs with predominant epithelial phenotype, self-renew and differentiate into mature cancer cells. Subsets of autophagic/ non-cyclic CSCs with predominant mesenchymal phenotype have capacity to invade, metastasize, resist to apoptosis, escape immunosurveillance, survive chemotherapies and are majorly responsible for cancer mortality. Differences in phenotypic plasticity may form the basis of differential impact of therapeutic outcomes on heterogeneous subpopulations of CSCs. Activation of autophagy is responsible for the recycling of damaged organelles and protein aggregates, regulates EMT, confers the survival advantage to neoplastic cells to anti-cancer therapies, significantly affects the invasive potential of cancer cells and supports their metastatic dissemination in a tissue and tumor stage dependent manner. Therapy resistance is the primary obstacle in the complete ablation of tumor cells. Combinational treatments based on targeting autophagic CSCs and inhibiting EMT regulators may represent potential anticancer strategies for the prevention of cancer invasion, metastatic spread and disease relapse.

中文翻译：

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上皮可塑性，自噬和转移：潜在的调节因子，可以克服治疗耐药性。

上皮到间充质转变（EMT）启动癌细胞的恶性转化，并负责生成癌症干细胞（CSC）的异源亚型。肿瘤微环境（TME）生态位内的环境线索和旁分泌因子形式的信号支持具有两个不同功能转变状态的CSC池生成的可能性。具有上皮表型的环状CSC自我更新并分化为成熟癌细胞。具有主要间充质表型的自噬/非环状CSC亚型具有侵袭，转移，抗凋亡，逃避免疫监视，生存化学疗法的能力，并且是造成癌症死亡的主要原因。表型可塑性的差异可能构成治疗结果对CSC异质亚群产生不同影响的基础。自噬的激活负责回收受损细胞器和蛋白质聚集体，调节EMT，赋予肿瘤细胞抗癌治疗的生存优势，显着影响癌细胞的侵袭潜能并支持其在组织和肿瘤阶段的转移性传播。依赖方式。治疗抵抗是肿瘤细胞完全消融的主要障碍。基于靶向自噬CSCs和抑制EMT调节剂的联合治疗可能代表了潜在的抗癌策略，可预防癌症的侵袭，转移扩散和疾病复发。自噬的激活负责回收受损细胞器和蛋白质聚集体，调节EMT，赋予肿瘤细胞抗癌治疗的生存优势，显着影响癌细胞的侵袭潜能并支持其在组织和肿瘤阶段的转移性传播。依赖方式。抗药性是肿瘤细胞完全消融的主要障碍。基于靶向自噬CSCs和抑制EMT调节剂的联合治疗可能代表了潜在的抗癌策略，可预防癌症的侵袭，转移扩散和疾病复发。自噬的激活负责回收受损细胞器和蛋白质聚集体，调节EMT，赋予肿瘤细胞抗癌治疗的生存优势，显着影响癌细胞的侵袭潜能并支持其在组织和肿瘤阶段的转移性传播。依赖方式。治疗抵抗是肿瘤细胞完全消融的主要障碍。基于靶向自噬CSCs和抑制EMT调节剂的联合治疗可能代表了潜在的抗癌策略，可预防癌症的侵袭，转移扩散和疾病复发。显着影响癌细胞的浸润潜能并以组织和肿瘤阶段依赖性的方式支持癌细胞的转移扩散。治疗抵抗是肿瘤细胞完全消融的主要障碍。基于靶向自噬CSCs和抑制EMT调节剂的联合治疗可能代表了潜在的抗癌策略，可预防癌症的侵袭，转移扩散和疾病复发。显着影响癌细胞的浸润潜能并以组织和肿瘤阶段依赖性的方式支持癌细胞的转移扩散。治疗抵抗是肿瘤细胞完全消融的主要障碍。基于靶向自噬CSCs和抑制EMT调节剂的联合治疗可能代表了潜在的抗癌策略，可预防癌症的侵袭，转移扩散和疾病复发。