About this Research Topic

Background

Cancer onset and progression is associated with a set of genomic, pathophysiologic, and phenotypic changes commonly referred to as the "Hallmarks of Cancer". On the cellular and tissue level, among the complex interplay of internal and extrinsic factors, the extracellular matrix (ECM), a structural component of most tissues, directly impacts the tumor microenvironment and consequently plays an important role in tumor malignancy by modulating tumor growth and migration. While the impact of ECM components on cellular behaviour can be related to their direct interaction with cell membranes and the underlying cytoskeleton, the network of ECM components can also impact inter-cellular communication and multicellular effects during tumorigenesis.

Even though research on ECMs is extensive, their role in different tissues, diseases, or biotechnological applications tends to be viewed separately. The fact that ECM composition is tissue-specific and that its functions may change accordingly most likely contributed to this separation, together with the general separation of inherited and acquired (e.g. neoplastic) variations in ECM components and their interaction partners. However, the profound role the ECM plays in a variety of contexts argues for an urgent need to combine the knowledge we have from different areas in an effort to identify common pathways. This can in turn help us to dissect out how ECM acts during normal physiological conditions and what changes when stress and damage arise in the context of disease, including cancer.

Stress and damage triggered either endogenously, for example, due to reactive oxygen species, or exogenously, for example, due to chemicals, lead to several events to ensure tissue repair, one of which is ECM remodeling. This remodeling not only acts to restructure the damaged area but also promotes, for example, the proliferation, differentiation, and migration of different cell types to restore function. In keeping with this, the use of decellularized matrix is a promising strategy in regenerative medicine, as it provides the optimal substrate for normal tissue repair and regeneration. On the negative side, since ECM remodeling promotes cell proliferation, migration and differentiation this will also provide the right environment for tumor development.

Mutations in genes that encode ECM components have been associated with different genetic disorders, including for example different muscular dystrophies, neurodegenerative disorders, Ehlers Danlos Syndromes, and osteogenesis imperfecta, and thus, stressing how important ECM is to maintain tissue homeostasis. However, how mutations in ECM components influence cancer progression has not been fully dissected yet.

Even though there is an increasing body of evidence, showing that ECM is critical to maintaining tissue homeostasis, the exact mechanisms and signaling pathways involved are not fully understood. The use of high throughput technologies, large scale bioinformatics or systems analyses or studies presenting generalized, multi-gene or integrative approaches may provide the missing links to uncover the pathways at the intersection between ECM components and cancer.This Research Topic aims at bringing together contributions on how the ECM plays a critical role in maintaining tissue homeostasis and countering disease development, with special emphasis on how ECM remodeling and mutations contribute to cancer. Overall the Topic should unravel new mechanisms and signaling pathways where ECM can be compared between normal and diseased states. For that authors are welcome to submit original articles, mini-reviews, or reviews considering the following subtopics:

- ECM and cancer
- ECM remodeling during stress and damage
- ECM and genetic disorders
- Decellularized ECM in disease treatment

Keywords: ECM

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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