Institute of Physiological Chemistry and Pathobiochemistry, University of Münster, Waldeyerstr. 15, 48149, Münster, Germany.
Clin Exp Metastasis. 2019 Jun;36(3):171-198. doi: 10.1007/s10585-019-09966-1. Epub 2019 Apr 11.
The extracellular matrix (ECM) constitutes the scaffold of tissues and organs. It is a complex network of extracellular proteins, proteoglycans and glycoproteins, which form supramolecular aggregates, such as fibrils and sheet-like networks. In addition to its biochemical composition, including the covalent intermolecular cross-linkages, the ECM is also characterized by its biophysical parameters, such as topography, molecular density, stiffness/rigidity and tension. Taking these biochemical and biophysical parameters into consideration, the ECM is very versatile and undergoes constant remodeling. This review focusses on this remodeling of the ECM under the influence of a primary solid tumor mass. Within this tumor stroma, not only the cancer cells but also the resident fibroblasts, which differentiate into cancer-associated fibroblasts (CAFs), modify the ECM. Growth factors and chemokines, which are tethered to and released from the ECM, as well as metabolic changes of the cells within the tumor bulk, add to the tumor-supporting tumor microenvironment. Metastasizing cancer cells from a primary tumor mass infiltrate into the ECM, which variably may facilitate cancer cell migration or act as barrier, which has to be proteolytically breached by the infiltrating tumor cell. The biochemical and biophysical properties therefore determine the rates and routes of metastatic dissemination. Moreover, primed by soluble factors of the primary tumor, the ECM of distant organs may be remodeled in a way to facilitate the engraftment of metastasizing cancer cells. Such premetastatic niches are responsible for the organotropic preference of certain cancer entities to colonize at certain sites in distant organs and to establish a metastasis. Translational application of our knowledge about the cancer-primed ECM is sparse with respect to therapeutic approaches, whereas tumor-induced ECM alterations such as increased tissue stiffness and desmoplasia, as well as breaching the basement membrane are hallmark of malignancy and diagnostically and histologically harnessed.
细胞外基质 (ECM) 构成组织和器官的支架。它是细胞外蛋白质、蛋白聚糖和糖蛋白的复杂网络,形成超分子聚集物,如纤维和片状网络。除了其生化组成,包括共价分子间交联,ECM 还具有生物物理参数,如形貌、分子密度、硬度/刚性和张力。考虑到这些生化和生物物理参数,ECM 非常多样化,并不断进行重塑。本综述重点介绍了原发性实体瘤对 ECM 的这种重塑。在这种肿瘤基质中,不仅癌细胞,而且分化为癌相关成纤维细胞 (CAF) 的常驻成纤维细胞也会改变 ECM。与 ECM 结合并从 ECM 释放的生长因子和趋化因子,以及肿瘤块内细胞的代谢变化,增加了支持肿瘤的肿瘤微环境。来自原发性肿瘤的转移癌细胞浸润 ECM,ECM 可不同程度地促进癌细胞迁移或作为屏障,需要浸润肿瘤细胞进行蛋白水解突破。因此,生化和生物物理特性决定了转移扩散的速度和途径。此外,由原发性肿瘤的可溶性因子启动,远处器官的 ECM 可能会重塑,以促进转移癌细胞的定植。这种预先存在的转移龛负责某些癌症实体在远处器官的特定部位定植和建立转移的器官倾向性。关于治疗方法,我们对癌症引发的 ECM 的知识的转化应用还很少,而肿瘤诱导的 ECM 改变,如组织硬度增加和纤维形成,以及基底膜的破坏,是恶性肿瘤的标志,并在诊断和组织学上得到利用。