This review discusses the role of extracellular matrix (ECM) remodelling in tumour progression and metastasis. Tumours exploit ECM remodelling to create a microenvironment that supports tumour growth and metastasis. The ECM is composed of various macromolecules, including collagens, proteoglycans, and glycoproteins, which are modified by enzymes such as oxidases and proteases. These modifications, along with the mechanical and topographical properties of the ECM, influence cell fate and function through mechanosignalling. The ECM has two main forms: the interstitial matrix, which provides structural integrity and modulates cell processes, and the basement membrane, which is a stable structure that lines epithelial and endothelial cells. Tumour cells and stromal cells modify the ECM through mechanisms such as deposition, chemical modification, proteolytic degradation, and force-mediated remodelling. These processes support tumour growth, increase cell migration, and remodel the ECM in distant organs to allow metastasis. ECM remodelling is essential for tissue homeostasis and wound healing but can be dysregulated in pathological conditions such as cancer. Tumour cells recruit and activate stromal cells, which deposit ECM components and support tumour growth. CAFs, a type of stromal cell, play a key role in ECM remodelling and can have both tumour-promoting and tumour-suppressive functions. ECM components such as hyaluronan and collagen have both tumour-suppressing and tumour-promoting properties, depending on their molecular weight and context. Tumour-secreted factors and stromal cells modify ECM components through post-translational modifications, which can influence cell signalling and tumour progression. ECM remodelling also supports tumour cell migration and invasion by altering the physical properties of the ECM and creating migratory tracks. Hypoxia promotes ECM remodelling and vascularisation, which is crucial for tumour growth and metastasis. The complex interplay between ECM remodelling and tumour progression highlights the importance of understanding these processes for developing therapeutic strategies targeting the ECM and its remodelling mechanisms.This review discusses the role of extracellular matrix (ECM) remodelling in tumour progression and metastasis. Tumours exploit ECM remodelling to create a microenvironment that supports tumour growth and metastasis. The ECM is composed of various macromolecules, including collagens, proteoglycans, and glycoproteins, which are modified by enzymes such as oxidases and proteases. These modifications, along with the mechanical and topographical properties of the ECM, influence cell fate and function through mechanosignalling. The ECM has two main forms: the interstitial matrix, which provides structural integrity and modulates cell processes, and the basement membrane, which is a stable structure that lines epithelial and endothelial cells. Tumour cells and stromal cells modify the ECM through mechanisms such as deposition, chemical modification, proteolytic degradation, and force-mediated remodelling. These processes support tumour growth, increase cell migration, and remodel the ECM in distant organs to allow metastasis. ECM remodelling is essential for tissue homeostasis and wound healing but can be dysregulated in pathological conditions such as cancer. Tumour cells recruit and activate stromal cells, which deposit ECM components and support tumour growth. CAFs, a type of stromal cell, play a key role in ECM remodelling and can have both tumour-promoting and tumour-suppressive functions. ECM components such as hyaluronan and collagen have both tumour-suppressing and tumour-promoting properties, depending on their molecular weight and context. Tumour-secreted factors and stromal cells modify ECM components through post-translational modifications, which can influence cell signalling and tumour progression. ECM remodelling also supports tumour cell migration and invasion by altering the physical properties of the ECM and creating migratory tracks. Hypoxia promotes ECM remodelling and vascularisation, which is crucial for tumour growth and metastasis. The complex interplay between ECM remodelling and tumour progression highlights the importance of understanding these processes for developing therapeutic strategies targeting the ECM and its remodelling mechanisms.