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Elucidating the role of matrix stiffness

So the aims of this chapter were to focus on extracellular matrix.

Invasion and metastatic skills, properties and functions of the ECM, abnormal ECM dynamics, tumor microenvironment and ECM, details of ECM invasion, role of ECM and ECM‐associated proteins in metastasis, tumor dormant and metastatic process, essential component of the niches, role of the ECM in tumor angiogenesis and lymphangiogenesis are be briefly explained in this chapter.

Abnormal ECM has profound impacts on surrounding cells, including epithelial, endothelial, and immune cells and other stromal cell types.

A cancer cell must complete a series of steps before it becomes a clinically detectable lesion for successful colonization in the body.

The interdispersed proteoglycans shows limited aggregation with hyaluronate (5).

It is restricted from swelling by an intact collagen network; (C) collagen fibers are degraded by two enzymatic pathways: (a) proteinases (i.e., cathepsins, elastase, plasmin, thrombin) act as “cross‐linkases” (4) to liberate collagen monomers from fibers (6).

At later stages when cancer cells awake from dormancy, abnormal ECM turns on the angiogenic switch (stage 8), presumably using a mechanism similar to that used at the primary site (stage 5), and promotes the rapid growth of cancer cells and an expansion of micrometastasis to macrometastasis (see ref. A couple of important properties of ECM are not illustrated in this cartoon.

First, ECMs are highly dynamic and can be modified by the cells that come into contact with them creating a bi‐directional mode of cell‐matrix communication.

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