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Scar/WAVE3 contributes to motility and plasticity of lamellipodial dynamics but not invasion in 3D

机译:疤痕/波浪3有助于层叠动力学的动力和可塑性但没有侵入3D

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摘要

The Scar/WAVE complex plays a major role in the motility of cells by activating the Arp2/3 complex, which initiates actin branching and drives protrusions. Mammals have three Scar/WAVE isoforms, which show some tissue specific expression, but their functions have not been differentiated. Here we show that depletion of the Scar/WAVE3 in the mammalian breast cancer cells MDA-MB-231 results in larger and less dynamic lamellipodia. Scar/WAVE3 depleted cells move more slowly but more persistently on a 2-dimensional matrix and they typically only show one lamellipod. However, Scar/WAVE3 appears to have no role in driving invasiveness in a 3D Matrigel invasion assay or a 3D collagen invasion assay, suggesting that lamellipodial persistence as seen in 2D is not crucial in 3D environments.
机译:Scar / WAVE复合物通过激活Arp2 / 3复合物在细胞运动中起主要作用,Arp2 / 3复合物引发肌动蛋白分支并驱动突起。哺乳动物具有三种Scar / WAVE同工型,它们表现出某些组织特异性表达,但其功能尚未区分。在这里,我们显示哺乳动物乳腺癌细胞MDA-MB-231中Scar / WAVE3的耗竭导致更大和更少动态的lamellipodia。疤痕/ WAVE3耗竭的细胞在二维矩阵上移动得更慢但更持久,它们通常仅显示一个lamellipod。但是,Scar / WAVE3在3D Matrigel入侵测定法或3D胶原入侵测定法中似乎没有驱动侵袭性的作用,表明在2D中看到的片状脂质体持久性在3D环境中并不关键。

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