School of Computer Science, Northwestern Polytechnical University, 1 Dongxiang Road, Chang'an District, Xi'an 710072, China.
Key Laboratory of Big Data Storage and Management, Northwestern Polytechnical University, Ministry of Industry and Information Technology, 1 Dongxiang Road, Chang'an District, Xi'an 710072, China.
Brief Bioinform. 2024 Sep 23;25(6). doi: 10.1093/bib/bbae603.
Lung adenocarcinoma, a prevalent subtype of lung cancer, represents one of the most lethal human malignancies. Despite substantial efforts to elucidate its biological underpinnings, the underlying mechanisms governing lung adenocarcinoma remain enigmatic. Modeling and comprehending the dynamics of gene regulatory networks are crucial for unraveling the fundamental mechanisms of lung adenocarcinoma. Conventionally, the cancer is modeled as an equilibrium process based on a time-invariant gene regulatory network to investigate stable cell states. However, the cancer is a nonequilibrium process and the gene regulatory network should be regarded as time-varying in actual. Therefore, a feasible framework was developed to explore the formation and progression of lung adenocarcinoma. On the one hand, to delve into the underlying mechanisms of lung adenocarcinoma formation, the time-invariant gene regulatory network for lung adenocarcinoma was initially undertaken, and the composition of stable cell states was elucidated based on landscape theory. Furthermore, the plasticity of different states was quantified using energy landscape decomposition theory by incorporating cell proliferation. And transition probabilities between different states were defined to elucidate the transition between stable cell states. Additionally, the global sensitivity analysis was performed and a total of three genes and three regulations were identified to be more critical for the formation lung adenocarcinoma, offering a novel strategy for designing network-based therapies for its treatment. On the other hand, the time-invariant gene regulatory network is extended as time-varying to delve into the underlying mechanisms of lung adenocarcinoma progression. The lung adenocarcinoma progression was characterized as four different disease stages based on the mixed states of cell population and the evolutionary direction. And the progressionary mechanism of transition between stages was expounded by evaluating their dynamical transport, with the dynamical transport cost between different stages quantified using Wasserstein metrics.
肺腺癌是一种常见的肺癌亚型,是人类最致命的恶性肿瘤之一。尽管人们已经做出了巨大的努力来阐明其生物学基础,但肺腺癌的潜在机制仍然是个谜。对基因调控网络的动态进行建模和理解,对于揭示肺腺癌的基本机制至关重要。传统上,基于时不变的基因调控网络,将癌症建模为一个平衡过程,以研究稳定的细胞状态。然而,癌症是一个非平衡过程,基因调控网络在实际中应该被视为时变的。因此,开发了一种可行的框架来探索肺腺癌的形成和进展。一方面,为了深入研究肺腺癌形成的潜在机制,首先进行了肺腺癌的时不变基因调控网络的研究,并基于景观理论阐明了稳定细胞状态的组成。此外,通过将细胞增殖纳入能量景观分解理论,量化了不同状态的可塑性。并定义了不同状态之间的跃迁概率,以阐明稳定细胞状态之间的跃迁。此外,进行了全局敏感性分析,确定了三个基因和三个调控,它们对于肺腺癌的形成更为关键,为基于网络的治疗方法提供了新的策略。另一方面,将时不变基因调控网络扩展为时变,以深入研究肺腺癌进展的潜在机制。根据细胞群体的混合状态和进化方向,将肺腺癌进展分为四个不同的疾病阶段。并通过评估它们的动力学输运来阐述不同阶段之间跃迁的进展机制,使用 Wasserstein 度量来量化不同阶段之间的动力学输运成本。