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arXiv 2112.03326physics.bio-phq-bio.CB
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高细胞密度下的自体趋化性

Autologous chemotaxis at high cell density

Michael Vennettilli, Louis Gonzalez, Nicholas Hilgert, Andrew Mugler

摘要:

细胞分泌和检测分子以确定流体流动方向的自主趋化性在高细胞密度下受阻,因为来自其他细胞的分子干扰给定细胞的信号。使用自体趋化性的极小模型,我们确定了传感失败的细胞密度,并发现它与转移性癌细胞的实验观察一致。为了理解这一协议,我们推导出一个物理限制自体趋化性的细胞密度,佩克莱数,和长度尺度的细胞和它的环境。令人惊讶的是,在信号分子均匀过饱和的环境中,我们发现传感不仅可能失败,而且可能被逆转,导致向后的细胞运动。我们的研究结果触及了化学和机械细胞传感之间竞争的核心,并阐明了癌细胞在密集肿瘤环境中采用的感觉策略。

英文摘要:

Autologous chemotaxis, in which cells secrete and detect molecules to determine the direction of fluid flow, is thwarted at high cell density because molecules from other cells interfere with a given cell's signal. Using a minimal model of autologous chemotaxis, we determine the cell density at which sensing fails and find that it agrees with experimental observations of metastatic cancer cells. To understand this agreement, we derive a physical limit to autologous chemotaxis in terms of the cell density, the Péclet number, and the length scales of the cell and its environment. Surprisingly, in an environment that is uniformly oversaturated in the signaling molecule, we find that sensing not only can fail, but can be reversed, causing backwards cell motion. Our results get to the heart of the competition between chemical and mechanical cellular sensing and shed light on a sensory strategy employed by cancer cells in dense tumor environments.

机构、总结、中文摘要均由AI分析而来,可能存在错误,请以论文正文为准。

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