**1. Introduction**

Extracellular matrix (ECM) was synthesized and secreted by embryonic cells starting from the early stages of its development. Our knowledge on the composition, structure, and function of ECM increased significantly in recent years. The most prominent among these is that extracel‐

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lular microenvironment holds a critical importance in cellular growth, survival, differentia‐ tion, and morphogenesis [1].

The major role played by the local microenvironment or niches in the arrangement of cellular behavior is gradually accepted more and more in cancer biology [2–5]. The fact that extracel‐ lular matrix is a dynamic source in the progression of cancer became the center of attention for researchers [1, 5–7].

ECM affects negatively multiple proteases in remodeling, but it should be debated whether proteolysis constitutes a mandatory step in tissue invasion [8]. Many groups reported that the crossed structural barriers of cancer cells may be transferred to ECM only via the proteolytic pathway. Yet, others suggested that the neoplastic cells progressed toward the matrix by pushing or suppressing without proteases [9–12]. No matter what the route is, neoplastic cells invade the two major subtypes of ECM, namely basal membrane and interstitium [13–17].
