The extracellular matrix (ECM) is a complex and dynamic network that provides structural support and regulates cellular behavior, which includes components such as fibrillar proteins, glycosaminoglycans, proteoglycans, and mucus. In recent years, the ECM has been recognized as one of the most important non-cellular components in the tumor microenvironment (TME), which remains relatively underexplored in immunology and tumor progression. Many studies have shown that the ECM highly influences TME by regulating immune cell recruitment, survival, and function, such as the migration of T cells. In turn, immune cells could directly or indirectly dictate ECM through the production of cytokines and chemokines (e.g., TGF-b, IL-13, CXCL4). For example, macrophages are pivotal in ECM remodeling through receptor (CD206)-mediated uptake and degradation of collagen. Moreover, the molecular mechanisms by which the pathological tumor ECM affects tumor therapy efficiency are still unclear. Therefore, exploring the complex relationship between ECM and immune cells in the TME during tumor progression may lead to the development of novel strategies for cancer treatments or the enhancement of the efficacy of tumor immunotherapy.
This Research Topic aims to highlight the complex interconnectivity between the ECM and immune cells in TME. It will cover topics ranging from the basic biology of the ECM to its effects on the immune cells, as well as its impact on tumor progression and the efficiency of tumor therapy. The goal is to provide insights into the mechanisms underlying the interactions between the ECM and immune cells and to develop new therapeutic targets/materials for cancer based on the ECM.
Original Research articles and Reviews are welcome. Subtopics include but are not limited to:
1) ECM-mediated modulation on immune cell recruitment and function in the TME (e.g. macrophages /T cells etc.);
2) Mechanism of chemokines, cytokines, and immune cells on ECM regulation/remodeling (e.g. TGF-ß/IL-13/MMP9, etc.);
3) ECM signaling pathways and their roles in tumor progression and metastasis;
4) Molecular mechanisms by which the ECM influences the efficacy of tumor immunotherapy (e.g. Cancer-associated fibroblasts/T cell trapping/Immunosuppressive signaling, etc.);
5) Designing ECM components-targeting materials for cancer target therapy (e.g. macrophages CD206-targeting nanoparticles/hyaluronic acid-based hydrogels, etc.);
6) Potential targets and combination therapeutic strategies based on the ECM and immune cells in TME.
Please NOTE: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of the scope for this section and will not be accepted as part of this Research Topic.
The extracellular matrix (ECM) is a complex and dynamic network that provides structural support and regulates cellular behavior, which includes components such as fibrillar proteins, glycosaminoglycans, proteoglycans, and mucus. In recent years, the ECM has been recognized as one of the most important non-cellular components in the tumor microenvironment (TME), which remains relatively underexplored in immunology and tumor progression. Many studies have shown that the ECM highly influences TME by regulating immune cell recruitment, survival, and function, such as the migration of T cells. In turn, immune cells could directly or indirectly dictate ECM through the production of cytokines and chemokines (e.g., TGF-b, IL-13, CXCL4). For example, macrophages are pivotal in ECM remodeling through receptor (CD206)-mediated uptake and degradation of collagen. Moreover, the molecular mechanisms by which the pathological tumor ECM affects tumor therapy efficiency are still unclear. Therefore, exploring the complex relationship between ECM and immune cells in the TME during tumor progression may lead to the development of novel strategies for cancer treatments or the enhancement of the efficacy of tumor immunotherapy.
This Research Topic aims to highlight the complex interconnectivity between the ECM and immune cells in TME. It will cover topics ranging from the basic biology of the ECM to its effects on the immune cells, as well as its impact on tumor progression and the efficiency of tumor therapy. The goal is to provide insights into the mechanisms underlying the interactions between the ECM and immune cells and to develop new therapeutic targets/materials for cancer based on the ECM.
Original Research articles and Reviews are welcome. Subtopics include but are not limited to:
1) ECM-mediated modulation on immune cell recruitment and function in the TME (e.g. macrophages /T cells etc.);
2) Mechanism of chemokines, cytokines, and immune cells on ECM regulation/remodeling (e.g. TGF-ß/IL-13/MMP9, etc.);
3) ECM signaling pathways and their roles in tumor progression and metastasis;
4) Molecular mechanisms by which the ECM influences the efficacy of tumor immunotherapy (e.g. Cancer-associated fibroblasts/T cell trapping/Immunosuppressive signaling, etc.);
5) Designing ECM components-targeting materials for cancer target therapy (e.g. macrophages CD206-targeting nanoparticles/hyaluronic acid-based hydrogels, etc.);
6) Potential targets and combination therapeutic strategies based on the ECM and immune cells in TME.
Please NOTE: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of the scope for this section and will not be accepted as part of this Research Topic.
