Maria Sklodowska-Curie National Research Institute of Oncology, Roentgena 5, 02-781 Warszawa, Poland.
Int J Mol Sci. 2022 Apr 30;23(9):4985. doi: 10.3390/ijms23094985.
Entosis-a homotypic insertion of one cell into another, resulting in a death of the invading cell-has been described in many reports, but crucial aspects of its molecular mechanisms and clinical significance still remain controversial. While actomyosin contractility of the invading cell is very well established as a driving force in the initial phase, and autophagy induced in the outer cell is determined as the main mechanism of degradation of the inner cell, many details remain unresolved. The multitude of triggering factors and crisscrossing molecular pathways described in entosis regulation make interpretations difficult. The question of the physiological role of entosis also remains unanswered. In this review, we summarize the knowledge of molecular mechanisms and clinical data concerning entosis accumulated so far, highlighting both coherent explanations and controversies.
细胞侵入（entosis）是指一个细胞侵入另一个细胞的过程，导致侵入细胞死亡。这种现象在许多报告中都有描述，但它的分子机制和临床意义的关键方面仍然存在争议。虽然侵入细胞的肌动球蛋白收缩力作为初始阶段的驱动力已得到充分证实，而外细胞中的自噬被确定为内细胞降解的主要机制，但仍有许多细节尚未解决。细胞侵入调节中描述的众多触发因素和交叉分子途径使得解释变得困难。细胞侵入的生理作用的问题也尚未得到解答。在这篇综述中，我们总结了迄今为止关于细胞侵入的分子机制和临床数据的知识，突出了一致的解释和争议。
