期刊
COMPUTATIONAL AND STRUCTURAL BIOTECHNOLOGY JOURNAL
卷 16, 期 -, 页码 237-245出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.csbj.2018.07.002
关键词
Mechanobiology; Cancer; Mathematical biology; Computational modelling; Signaling; Cytoskeleton; Focal adhesions; Mechanotransduction
资金
- Yale University
- Stand Up to Cancer Campaign for Cancer Research UK via a Programme Foundation Award [C37275/A20146]
Mechanics and biochemical signaling are both often deregulated in cancer, leading to increased cell invasiveness, proliferation, and survival. The dynamics and interactions of cytoskeletal components control basic mechanical properties, such as cell tension, stiffness, and engagement with the extracellular environment, which can lead to extracellular matrix remodeling. Intracellular mechanics can alter signaling and transcription factors, impacting cell decision making. Additionally, signaling from soluble and mechanical factors in the extracellular environment, such as substrate stiffness and ligand density, can modulate cytoskeletal dynamics. Computational models closely integrated with experimental support, incorporating cancer-specific parameters, can provide quantitative assessments and serve as predictive tools toward dissecting the feedback between signaling and mechanics and across multiple scales and domains in tumor progression. (c) 2018 The Authors. Published by Elsevier B.V. on behalf of Research Network of Computational and Structural Biotechnology. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
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