The extracellular matrix (ECM) plays a crucial role in tumor progression and metastasis through its dynamic remodeling. Tumors exploit the ECM to create a microenvironment that promotes tumor growth and metastasis. This review focuses on how tumor cells and stromal cells deposit, modify, and degrade the ECM, which supports tumor growth, increases cell migration, and remodels distant organs to facilitate metastasis. Understanding these mechanisms is essential for developing therapeutic treatments. The ECM consists of various macromolecules, including collagens, proteoglycans, and glycoproteins, which can be modified post-translationally by enzymes like oxidases and proteases. These modifications alter the biochemical and biophysical properties of the ECM, affecting cell signaling, proliferation, differentiation, migration, and apoptosis. The ECM has two main forms: the interstitial matrix and the basement membrane, each with distinct functions and compositions. ECM remodelling involves four main processes: deposition, chemical modification, proteolytic degradation, and force-mediated physical remodelling. Tumor cells and stromal cells, particularly cancer-associated fibroblasts (CAFs), activate these processes to create a cancer-supporting matrix. CAFs, derived from various cell types, secrete large amounts of ECM components and modify their structure, increasing matrix stiffness and creating barriers to immune surveillance. ECM components have both tumor-suppressing and tumor-promoting properties. For example, hyaluronan (HA) can act as a tumor suppressor or promoter depending on its molecular weight. Increased deposition of fibrillar collagen and other ECM components leads to a fibrotic phenotype, desmoplasia, which is associated with poor prognosis in various cancers. Proteolytic degradation of the ECM by MMPs and other proteases releases bioactive fragments and growth factors, promoting tumor progression. These fragments can also induce further ECM degradation, creating a vicious cycle. The physical properties of the ECM, such as stiffness, influence tumor cell migration and invasion. Hypoxia triggers ECM remodelling through HIF-1 signaling, promoting angiogenesis and metastasis. During metastasis, the ECM remodels to support the survival and dissemination of circulating tumor cells (CTCs). Understanding these complex mechanisms is crucial for developing targeted therapies to prevent and eliminate cancer metastasis.The extracellular matrix (ECM) plays a crucial role in tumor progression and metastasis through its dynamic remodeling. Tumors exploit the ECM to create a microenvironment that promotes tumor growth and metastasis. This review focuses on how tumor cells and stromal cells deposit, modify, and degrade the ECM, which supports tumor growth, increases cell migration, and remodels distant organs to facilitate metastasis. Understanding these mechanisms is essential for developing therapeutic treatments. The ECM consists of various macromolecules, including collagens, proteoglycans, and glycoproteins, which can be modified post-translationally by enzymes like oxidases and proteases. These modifications alter the biochemical and biophysical properties of the ECM, affecting cell signaling, proliferation, differentiation, migration, and apoptosis. The ECM has two main forms: the interstitial matrix and the basement membrane, each with distinct functions and compositions. ECM remodelling involves four main processes: deposition, chemical modification, proteolytic degradation, and force-mediated physical remodelling. Tumor cells and stromal cells, particularly cancer-associated fibroblasts (CAFs), activate these processes to create a cancer-supporting matrix. CAFs, derived from various cell types, secrete large amounts of ECM components and modify their structure, increasing matrix stiffness and creating barriers to immune surveillance. ECM components have both tumor-suppressing and tumor-promoting properties. For example, hyaluronan (HA) can act as a tumor suppressor or promoter depending on its molecular weight. Increased deposition of fibrillar collagen and other ECM components leads to a fibrotic phenotype, desmoplasia, which is associated with poor prognosis in various cancers. Proteolytic degradation of the ECM by MMPs and other proteases releases bioactive fragments and growth factors, promoting tumor progression. These fragments can also induce further ECM degradation, creating a vicious cycle. The physical properties of the ECM, such as stiffness, influence tumor cell migration and invasion. Hypoxia triggers ECM remodelling through HIF-1 signaling, promoting angiogenesis and metastasis. During metastasis, the ECM remodels to support the survival and dissemination of circulating tumor cells (CTCs). Understanding these complex mechanisms is crucial for developing targeted therapies to prevent and eliminate cancer metastasis.