Division of Molecular Medicine & Genetics, Department of Internal Medicine, and the Life Sciences Institute, University of Michigan, Ann Arbor, Michigan, USA.
J Microsc. 2013 Sep;251(3):250-60. doi: 10.1111/jmi.12064.
During development, wound repair and disease-related processes, such as cancer, normal, or neoplastic cell types traffic through the extracellular matrix (ECM), the complex composite of collagens, elastin, glycoproteins, proteoglycans, and glycosaminoglycans that dictate tissue architecture. Current evidence suggests that tissue-invasive processes may proceed by protease-dependent or protease-independent strategies whose selection is not only governed by the characteristics of the motile cell population, but also by the structural properties of the intervening ECM. Herein, we review the mechanisms by which ECM dimensionality, elasticity, crosslinking, and pore size impact patterns of cell invasion. This summary should prove useful when designing new experimental approaches for interrogating invasion programs as well as identifying potential cellular targets for next-generation therapeutics.
在发育、伤口修复和疾病相关过程中，如癌症，正常或肿瘤细胞类型通过细胞外基质（ECM）迁移，ECM 是胶原蛋白、弹性蛋白、糖蛋白、蛋白聚糖和糖胺聚糖的复杂组合，决定组织架构。目前的证据表明，组织侵袭过程可能通过依赖蛋白酶或不依赖蛋白酶的策略进行，其选择不仅取决于迁移细胞群体的特征，还取决于中间 ECM 的结构特性。本文综述了 ECM 维度、弹性、交联和孔径如何影响细胞侵袭模式的机制。在设计用于研究侵袭程序的新实验方法以及确定下一代治疗药物的潜在细胞靶标时，本综述应证明是有用的。
