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Proteolysis-free amoeboid migration of melanoma cells through crowded environments via bleb-driven worrying
Developmental Cell ( IF 10.7 ) Pub Date : 2024-06-12 , DOI: 10.1016/j.devcel.2024.05.024 Meghan K. Driscoll , Erik S. Welf , Andrew Weems , Etai Sapoznik , Felix Zhou , Vasanth S. Murali , Juan Manuel García-Arcos , Minna Roh-Johnson , Matthieu Piel , Kevin M. Dean , Reto Fiolka , Gaudenz Danuser
Developmental Cell ( IF 10.7 ) Pub Date : 2024-06-12 , DOI: 10.1016/j.devcel.2024.05.024 Meghan K. Driscoll , Erik S. Welf , Andrew Weems , Etai Sapoznik , Felix Zhou , Vasanth S. Murali , Juan Manuel García-Arcos , Minna Roh-Johnson , Matthieu Piel , Kevin M. Dean , Reto Fiolka , Gaudenz Danuser
In crowded microenvironments, migrating cells must find or make a path. Amoeboid cells are thought to find a path by deforming their bodies to squeeze through tight spaces. Yet, some amoeboid cells seem to maintain a near-spherical morphology as they move. To examine how they do so, we visualized amoeboid human melanoma cells in dense environments and found that they carve tunnels via bleb-driven degradation of extracellular matrix components without the need for proteolytic degradation. Interactions between adhesions and collagen at the cell front induce a signaling cascade that promotes bleb enlargement via branched actin polymerization. Large blebs abrade collagen, creating feedback between extracellular matrix structure, cell morphology, and polarization that enables both path generation and persistent movement.
中文翻译:
黑色素瘤细胞通过气泡驱动的担忧在拥挤环境中的无蛋白水解变形虫迁移
在拥挤的微环境中,迁移的细胞必须找到或开辟一条路径。变形虫细胞被认为通过变形身体来挤过狭小空间来找到路径。然而,一些变形虫细胞在移动时似乎保持着接近球形的形态。为了研究它们是如何做到这一点的,我们在密集的环境中观察了变形虫类人类黑色素瘤细胞,发现它们通过 Bleb 驱动的细胞外基质成分降解来切割隧道,而无需蛋白水解降解。细胞前部粘附物和胶原蛋白之间的相互作用诱导信号级联反应,通过支链肌动蛋白聚合促进气泡扩大。大气泡磨损胶原蛋白,在细胞外基质结构、细胞形态和极化之间产生反馈,从而实现路径生成和持续运动。
更新日期:2024-06-12
中文翻译:
黑色素瘤细胞通过气泡驱动的担忧在拥挤环境中的无蛋白水解变形虫迁移
在拥挤的微环境中,迁移的细胞必须找到或开辟一条路径。变形虫细胞被认为通过变形身体来挤过狭小空间来找到路径。然而,一些变形虫细胞在移动时似乎保持着接近球形的形态。为了研究它们是如何做到这一点的,我们在密集的环境中观察了变形虫类人类黑色素瘤细胞,发现它们通过 Bleb 驱动的细胞外基质成分降解来切割隧道,而无需蛋白水解降解。细胞前部粘附物和胶原蛋白之间的相互作用诱导信号级联反应,通过支链肌动蛋白聚合促进气泡扩大。大气泡磨损胶原蛋白,在细胞外基质结构、细胞形态和极化之间产生反馈,从而实现路径生成和持续运动。