Sundstrom Andrew, Bar-Sagi Dafna, Mishra Bud
Department of Pharmacology and Systems Therapeutics, Icahn School of Medicine at Mount Sinai, New York, NY, United States of America.
Department of Computer Science, Courant Institute of Mathematical Sciences, New York, NY, United States of America.
PLoS One. 2016 Dec 28;11(12):e0168984. doi: 10.1371/journal.pone.0168984. eCollection 2016.
Certain tumor phenomena, like metabolic heterogeneity and local stable regions of chronic hypoxia, signify a tumor's resistance to therapy. Although recent research has shed light on the intracellular mechanisms of cancer metabolic reprogramming, little is known about how tumors become metabolically heterogeneous or chronically hypoxic, namely the initial conditions and spatiotemporal dynamics that drive these cell population conditions. To study these aspects, we developed a minimal, spatially-resolved simulation framework for modeling tissue-scale mixed populations of cells based on diffusible particles the cells consume and release, the concentrations of which determine their behavior in arbitrarily complex ways, and on stochastic reproduction. We simulate cell populations that self-sort to facilitate metabolic symbiosis, that grow according to tumor-stroma signaling patterns, and that give rise to stable local regions of chronic hypoxia near blood vessels. We raise two novel questions in the context of these results: (1) How will two metabolically symbiotic cell subpopulations self-sort in the presence of glucose, oxygen, and lactate gradients? We observe a robust pattern of alternating striations. (2) What is the proper time scale to observe stable local regions of chronic hypoxia? We observe the stability is a function of the balance of three factors related to O2-diffusion rate, local vessel release rate, and viable and hypoxic tumor cell consumption rate. We anticipate our simulation framework will help researchers design better experiments and generate novel hypotheses to better understand dynamic, emergent whole-tumor behavior.
某些肿瘤现象,如代谢异质性和慢性缺氧的局部稳定区域,表明肿瘤对治疗具有抗性。尽管最近的研究揭示了癌症代谢重编程的细胞内机制,但对于肿瘤如何变得代谢异质性或慢性缺氧,即驱动这些细胞群体状态的初始条件和时空动态,我们知之甚少。为了研究这些方面,我们开发了一个最小化的、具有空间分辨率的模拟框架,用于基于细胞消耗和释放的可扩散粒子对组织尺度的混合细胞群体进行建模,这些粒子的浓度以任意复杂的方式决定细胞行为,并基于随机繁殖。我们模拟了能够自我分类以促进代谢共生、根据肿瘤-基质信号模式生长并在血管附近产生慢性缺氧稳定局部区域的细胞群体。基于这些结果,我们提出了两个新问题:(1)在存在葡萄糖、氧气和乳酸梯度的情况下,两个代谢共生的细胞亚群将如何自我分类?我们观察到一种稳健的交替条纹模式。(2)观察慢性缺氧稳定局部区域的合适时间尺度是多少?我们观察到稳定性是与氧气扩散速率、局部血管释放速率以及存活和缺氧肿瘤细胞消耗速率相关的三个因素平衡的函数。我们预计我们的模拟框架将帮助研究人员设计更好的实验并产生新的假设,以更好地理解动态的、涌现的全肿瘤行为。