The tumor microenvironment has become increasingly important in recent decades of cancer research. Its key component, the extracellular matrix (ECM), has been shown to play a critical role in oncogenesis, angiogenesis, epithelial-mesenchymal transition, metastasis and resistance mechanisms to several therapies. Cellular functions and processes involved in cancer are indeed impacted by a complex network of structural proteins, of which three major classes involve: adhesive proteins such as collagens, proteoglycans, and glycoproteins. Many of these macromolecules are targeted by proteolytic processes including the activity of matrix metalloproteinases. Among the adhesive proteins, collagen, in particular, can undergo enzymatic and non-enzymatic modifications which result in the remodeling of its organization. Cellular receptors play a crucial role in the cross-talk between ECM and cancer cells as they are able to interact specifically with various components of ECM, such as adhesive components and soluble factors, to trigger specific cellular signaling which will subsequently impact the phenotype of the tumor. Both stromal and tumor cells secrete soluble factors that can further modulate this cross-talk.
The objective of this Research Topic is to review the recent data, in terms of molecular and cellular mechanisms involved in the dialogue between ECM and cancer cells, and consequently in tumor phenotype (proliferation, cell death, cell dormancy, angiogenesis, epithelial-mesenchymal transition, migration, invasion, and response to therapy). We would like to discuss different physiopathological conditions that lead to the alteration of the biochemical and biophysical properties of ECM (biochemical modifications, remodeling, modulation, and degradation), which results in deep changes in its mechanical properties (stiffness, density, and topology). These changes are able to affect the cellular mechanosensing and consequently the progression of the disease.
In this Research Topic we welcome Original Research, Review and Mini-Review articles focusing on:
1) ECM macromolecules (for example collagens, fibronectin, elastin, laminin, Tenascins, glycosaminoglycans, thrombospondins).
2) Cellular receptors of ECM (for example integrins and discoidin domain receptors).
3) Modulation of the ECM receptors activity (cleavage, co-receptors, recycling).
4) ECM remodeling (aging, obesity, fibrosis, Lysyl oxidase, proteolytic processes).
5) Active fragments from the degradation of ECM (matrikines, matricryptins).
6) Stromal and tumor cell-derived soluble factors (growth factors, cytokines, chemokines).
7) Targeting the ECM and cellular receptors dialogue (small molecules, mimetic peptides, antibodies).
The tumor microenvironment has become increasingly important in recent decades of cancer research. Its key component, the extracellular matrix (ECM), has been shown to play a critical role in oncogenesis, angiogenesis, epithelial-mesenchymal transition, metastasis and resistance mechanisms to several therapies. Cellular functions and processes involved in cancer are indeed impacted by a complex network of structural proteins, of which three major classes involve: adhesive proteins such as collagens, proteoglycans, and glycoproteins. Many of these macromolecules are targeted by proteolytic processes including the activity of matrix metalloproteinases. Among the adhesive proteins, collagen, in particular, can undergo enzymatic and non-enzymatic modifications which result in the remodeling of its organization. Cellular receptors play a crucial role in the cross-talk between ECM and cancer cells as they are able to interact specifically with various components of ECM, such as adhesive components and soluble factors, to trigger specific cellular signaling which will subsequently impact the phenotype of the tumor. Both stromal and tumor cells secrete soluble factors that can further modulate this cross-talk.
The objective of this Research Topic is to review the recent data, in terms of molecular and cellular mechanisms involved in the dialogue between ECM and cancer cells, and consequently in tumor phenotype (proliferation, cell death, cell dormancy, angiogenesis, epithelial-mesenchymal transition, migration, invasion, and response to therapy). We would like to discuss different physiopathological conditions that lead to the alteration of the biochemical and biophysical properties of ECM (biochemical modifications, remodeling, modulation, and degradation), which results in deep changes in its mechanical properties (stiffness, density, and topology). These changes are able to affect the cellular mechanosensing and consequently the progression of the disease.
In this Research Topic we welcome Original Research, Review and Mini-Review articles focusing on:
1) ECM macromolecules (for example collagens, fibronectin, elastin, laminin, Tenascins, glycosaminoglycans, thrombospondins).
2) Cellular receptors of ECM (for example integrins and discoidin domain receptors).
3) Modulation of the ECM receptors activity (cleavage, co-receptors, recycling).
4) ECM remodeling (aging, obesity, fibrosis, Lysyl oxidase, proteolytic processes).
5) Active fragments from the degradation of ECM (matrikines, matricryptins).
6) Stromal and tumor cell-derived soluble factors (growth factors, cytokines, chemokines).
7) Targeting the ECM and cellular receptors dialogue (small molecules, mimetic peptides, antibodies).
