细胞外基质
机械敏感通道
表型
胶质母细胞瘤
表观遗传学
变硬
肿瘤微环境
机械转化
肿瘤进展
细胞生物学
刚度
生物
入侵足纲
细胞外
表型转换
癌症研究
转录因子
基质(化学分析)
下调和上调
神经科学
化学
机械生物学
病态的
癌细胞
细胞
医学
癌症
基质金属蛋白酶
中间灯丝
细胞骨架
细胞内
循环肿瘤细胞
静脉注射
肿瘤细胞
作者
Paola Suarez Meade,Rachel Whitehead,Steve Rosenfeld,Paula Schiapparelli,Κωνσταντίνος Κωνσταντόπουλος,Alfredo Quiñones‐Hinojosa
出处
期刊:Neuro-oncology
[Oxford University Press]
日期:2025-09-13
卷期号:28 (1): 19-37
被引量:7
标识
DOI:10.1093/neuonc/noaf205
摘要
Extracellular matrix (ECM) stiffening correlates with tumor invasion in various cancer types, including glioblastoma (GBM). Increased matrix stiffness promotes a migratory phenotype through dysregulation of cell-ECM bidirectional communication. Exposure to stiffer environments is sensed by cells, which then adapt in ways that promote invasive behavior. These adaptive changes are imprinted onto the cells and persist even after they are placed in new, softer microenvironments via a process known as "mechanical memory." Mechanical memory is believed to be driven by mechanosensitive transcription factor activity and epigenetic remodeling. Glioblastoma recurrence is linked to the ability of cells to disperse and infiltrate the surrounding healthy tissue. Extracellular matrix stiffness in GBM is heterogeneous; it starts with a softer tumor core and becomes progressively stiffer toward the tumor's edges, potentially promoting sustained tumor invasion through mechanical memory. This review discusses the role of ECM stiffness in cancer cell behavior and the implications of ECM stiffening in GBM. We then describe the findings associated with mechanical memory and relay underlying mechanisms currently understood to drive the preservation of mechanically primed phenotypes. Finally, we discuss how matrix stiffness can drive migratory phenotypes in GBM cells and the potential role that progressive ECM dysregulation at the tumor periphery can link the formation of invasive tumor niches to the aggressive, resistant, and mesenchymal-like phenotypes present in GBM recurrent tumors.
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