恶性肿瘤细胞可塑性是肿瘤生物学的重要标志，对于转移和耐药性至关重要。细胞可塑性让癌细胞适应并逃避治疗策略，这是癌症患者死亡的主要原因。上皮细胞通过上皮-间质转化（EMT）获得迁移性，而间充质细胞通过间充质-阿米巴转化（MAT）获得阿米巴特征，从而增强其迁移能力和克隆形成潜力。肿瘤的形成、进展和转移取决于肿瘤微环境（TME），即肿瘤内部和周围的复杂生态系统。通过增加癌细胞的迁移和转移，TME 也会导致恶性肿瘤。本综述强调了入侵模式形态表现与 TME 内发现的不同结构之间的区别。此外，还讨论了变形虫相关特征促进耐药和转移的机制，以及这些机制如何代表治疗机会。版权所有 © 2024。由 Elsevier B.V. 出版。

Malignant cell plasticity is an important hallmark of tumor biology and crucial for metastasis and resistance. Cell plasticity lets cancer cells adapt to and escape the therapeutic strategies, which is the leading cause of cancer patient mortality. Epithelial cells acquire mobility via epithelial-mesenchymal transition (EMT), whereas mesenchymal cells enhance their migratory ability and clonogenic potential by acquiring amoeboid characteristics through mesenchymal-amoeboid transition (MAT). Tumor formation, progression, and metastasis depend on the tumor microenvironment (TME), a complex ecosystem within and around a tumor. Through increased migration and metastasis of cancer cells, the TME also contributes to malignancy. This review underscores the distinction between invasion pattern morphological manifestations and the diverse structures found within the TME. Furthermore, the mechanisms by which amoeboid-associated characteristics promote resistance and metastasis and how these mechanisms may represent therapeutic opportunities are discussed.Copyright © 2024. Published by Elsevier B.V.