Graduate Program in Computational and Systems Biology, Oswaldo Cruz Institute (IOC), Oswaldo Cruz Foundation (FIOCRUZ), Rio de Janeiro 21040-900, Brazil.
Department of Applied Mathematics, Institute of Mathematics, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro 21941-909, Brazil.
Int J Mol Sci. 2024 Apr 30;25(9):4894. doi: 10.3390/ijms25094894.
Glioblastoma Multiforme is a brain tumor distinguished by its aggressiveness. We suggested that this aggressiveness leads single-cell RNA-sequence data (scRNA-seq) to span a representative portion of the cancer attractors domain. This conjecture allowed us to interpret the scRNA-seq heterogeneity as reflecting a representative trajectory within the attractor's domain. We considered factors such as genomic instability to characterize the cancer dynamics through stochastic fixed points. The fixed points were derived from centroids obtained through various clustering methods to verify our method sensitivity. This methodological foundation is based upon sample and time average equivalence, assigning an interpretative value to the data cluster centroids and supporting parameters estimation. We used stochastic simulations to reproduce the dynamics, and our results showed an alignment between experimental and simulated dataset centroids. We also computed the Waddington landscape, which provided a visual framework for validating the centroids and standard deviations as characterizations of cancer attractors. Additionally, we examined the stability and transitions between attractors and revealed a potential interplay between subtypes. These transitions might be related to cancer recurrence and progression, connecting the molecular mechanisms of cancer heterogeneity with statistical properties of gene expression dynamics. Our work advances the modeling of gene expression dynamics and paves the way for personalized therapeutic interventions.
胶质母细胞瘤是一种侵袭性很强的脑肿瘤。我们提出,这种侵袭性导致单细胞 RNA 测序数据 (scRNA-seq) 跨越癌症吸引子域的代表性部分。这一猜想使我们能够将 scRNA-seq 的异质性解释为反映吸引子域内的代表性轨迹。我们考虑了基因组不稳定性等因素,通过随机固定点来描述癌症动力学。这些固定点是从通过各种聚类方法获得的质心中得出的,以验证我们方法的敏感性。这种方法学基础基于样本和时间平均等效性,为数据聚类质心和支持参数估计赋予解释值。我们使用随机模拟来重现动力学,我们的结果显示实验数据集和模拟数据集质心之间存在一致性。我们还计算了 Waddington 景观,为验证质心和标准偏差作为癌症吸引子的特征提供了一个可视化框架。此外,我们还研究了吸引子之间的稳定性和转换,揭示了潜在的亚型相互作用。这些转变可能与癌症复发和进展有关,将癌症异质性的分子机制与基因表达动力学的统计特性联系起来。我们的工作推进了基因表达动力学的建模,并为个性化治疗干预铺平了道路。