The effect of glucose restriction on cancer cell contractility: A threshold response in U-87 glioma

Albert Kong, Alessia Pallaoro, Donald Yapp, Gwynn J Elfring, Mattia Bacca
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Abstract

Cells rely on contractility to proliferate, and cancerous ones exhibit an increased glucose dependence. It is therefore hypothesized that glucose restriction can mitigate cancer cell proliferation by stunting their contractility. However, glucose-restriction studies have mostly been based on experiments that have yielded conflicting results; some cells become less contractile under glucose-restriction, intuitively, while, others become surprisingly more contractile. Active mechanistic modeling may prove fruitful in resolving these conflicts. In this study, we develop a model for glucose-mediated cell contractility to capture the mechanical implications of glucose restriction. The model is calibrated on cell contraction data taken from 2D-cultured glioma cells, laying on a collagen substrate. The model predicts the existence of a critical level of glucose restriction that must be exceeded for contractility to be affected, and this is validated by our experiments. Our model provides an initial step toward a fundamental understanding of the metabolic implications of cell contractility, particularly in the context of glucose restriction: an essential step in cancer studies.
葡萄糖限制对癌细胞收缩力的影响:U-87 胶质瘤的阈值反应
细胞依靠收缩力来增殖,而癌细胞对葡萄糖的依赖性更强。因此,人们假设限制葡萄糖可以通过阻碍癌细胞的收缩力来减缓癌细胞的增殖。然而,葡萄糖限制研究大多以实验为基础,实验结果相互矛盾;直观地看,一些细胞在葡萄糖限制下收缩力减弱,而另一些细胞却出人意料地收缩力增强。积极的机理建模可能有助于解决这些矛盾。在本研究中,我们建立了一个葡萄糖介导的细胞收缩性模型,以捕捉葡萄糖限制的机械影响。该模型根据铺设在胶原基底上的二维培养胶质瘤细胞的收缩数据进行校准。该模型预测存在一个临界葡萄糖限制水平,必须超过该水平才会影响细胞收缩,我们的实验也验证了这一点。我们的模型为从根本上理解细胞收缩性的代谢影响,特别是在葡萄糖限制的情况下,迈出了第一步:这是癌症研究中必不可少的一步。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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