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细胞外基质重塑与缺氧信号在调控癌症转移中的生物物理相互作用

Biophysical interplay between extracellular matrix remodeling and hypoxia signaling in regulating cancer metastasis.

作者信息

Lee Sun-Ah, Cho Gi-Ju, Kim Doyoung, Kim Dong-Hwee

机构信息

KU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul, Republic of Korea.

Department of Integrative Energy Engineering, College of Engineering, Korea University, Seoul, Republic of Korea.

出版信息

Front Cell Dev Biol. 2024 Mar 13;12:1335636. doi: 10.3389/fcell.2024.1335636. eCollection 2024.

DOI:10.3389/fcell.2024.1335636
PMID:38544822
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10965814/
Abstract

Mechanical properties of the tumor microenvironment play a critical role in cancer progression by activation of cancer mechano-responses. The biophysical interactions between cancer cells and their dynamic microenvironment are attributed to force-dependent alterations in molecular pathways that trigger the structural reorganization of intracellular organelles and their associated genetic modifications. Recent studies underscore the role of oxygen concentration in cancer metastasis. Suppressed oxygen levels promote the development of invasive phenotypes and aggressive proliferation of cancer cells, accompanied by remodeling of tumor microenvironment encompassing the modulation of physical settings of extracellular matrix. This review summarizes the role of biophysical interactions between cancer cells and their surroundings in determining cancer progression. Biophysical interpretation of the tumor microenvironment and cancer progression could provide further insights into the development of novel biomedical technologies for therapeutic cancer treatment.

摘要

肿瘤微环境的力学特性通过激活癌症机械反应在癌症进展中起关键作用。癌细胞与其动态微环境之间的生物物理相互作用归因于分子途径中依赖力的改变，这些改变触发细胞内细胞器的结构重组及其相关的基因修饰。最近的研究强调了氧浓度在癌症转移中的作用。低氧水平促进侵袭性表型的发展和癌细胞的侵袭性增殖，同时伴随着肿瘤微环境的重塑，包括细胞外基质物理环境的调节。本综述总结了癌细胞与其周围环境之间的生物物理相互作用在决定癌症进展中的作用。对肿瘤微环境和癌症进展的生物物理解释可为开发新型癌症治疗生物医学技术提供进一步的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c2/10965814/dad03d95d8ae/fcell-12-1335636-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c2/10965814/117111e5e5f4/fcell-12-1335636-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c2/10965814/ca3586996c70/fcell-12-1335636-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c2/10965814/5e8cb4bb4508/fcell-12-1335636-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c2/10965814/513c0b51bd78/fcell-12-1335636-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c2/10965814/dad03d95d8ae/fcell-12-1335636-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c2/10965814/117111e5e5f4/fcell-12-1335636-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c2/10965814/ca3586996c70/fcell-12-1335636-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c2/10965814/5e8cb4bb4508/fcell-12-1335636-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c2/10965814/513c0b51bd78/fcell-12-1335636-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c2/10965814/dad03d95d8ae/fcell-12-1335636-g005.jpg

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