Cell migration is essential to most living organisms. Single cell migration involves two distinct mechanisms, either a focal adhesion- and traction-dependent mesenchymal motility or an adhesion-independent but contractility-driven propulsive amoeboid locomotion. Cohesive migration of a group of cells, also called collective cell migration, has been only described as an adhesion- and traction-dependent mode of locomotion where the driving forces are mostly exerted at the front by leader cells. Here, by studying primary cancer specimens and cell lines from colorectal cancer, we demonstrate the existence of a second mode of collective migration which does not require adhesion to the surroundings and relies on a polarised supracellular contractility. Cell clusters confined into non-adhesive microchannels migrate in a rounded morphology, independently of the formation of focal adhesions or protruding leader cells, and lacking internal flow of cells, ruling-out classical traction-driven collective migration. Like single cells migrating in an amoeboid fashion, the clusters display a supracellular actin cortex with myosin II enriched at the rear. Using pharmacological inhibitors and optogenetics, we show that this polarised actomyosin activity powers migration and propels the clusters. This new mode of migration, that we named collective amoeboid, could be enabled by intrinsic or extrinsic neoplasic features to enable the metastatic spread of cancers.

中文翻译：

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细胞团在密闭的非粘性环境中采用集体的变形虫迁移模式

细胞迁移对于大多数生物都是必不可少的。单细胞迁移涉及两种不同的机制，即局灶性黏附和牵引依赖性间充质运动或黏附非依赖性但可收缩性驱动的推进性类运动。一组细胞的内聚性迁移，也称为集体细胞迁移，仅被描述为一种依赖于粘附和牵引力的运动方式，其中驱动力主要由前导细胞施加在前部。在这里，通过研究来自结肠直肠癌的原发癌标本和细胞系，我们证明了存在第二种集体迁移模式，该模式不需要粘附至周围环境，而是依赖于极化的超细胞收缩性。局限于非粘附性微通道的细胞簇以圆形形态迁移，与局灶性粘连或突出的前导细胞的形成无关，并且缺乏细胞的内部流动，排除了经典牵引驱动的集体迁移。像单细胞以类动植物的方式迁移一样，这些簇显示出一个细胞上肌动蛋白皮层，其后部富含肌球蛋白II。使用药理抑制剂和光遗传学，我们表明这种极化的放线菌素活性为迁移提供动力并推动了簇。这种新的迁移方式（我们称为集体变形虫）可以通过固有的或非固有的赘生性特征来实现，以实现癌症的转移性扩散。簇显示出一个细胞上肌动蛋白皮质，其后部富含肌球蛋白II。使用药理学抑制剂和光遗传学，我们表明这种极化的放线菌素活性为迁移提供动力并推动了簇。这种新的迁移方式（我们称为集体变形虫）可以通过固有的或非固有的赘生性特征来实现，以实现癌症的转移性扩散。簇显示出一个细胞上肌动蛋白皮质，其后部富含肌球蛋白II。使用药理学抑制剂和光遗传学，我们表明这种极化的放线菌素活性为迁移提供动力并推动了簇。这种新的迁移方式（我们称为集体变形虫）可以通过固有的或非固有的赘生性特征来实现，以实现癌症的转移性扩散。