Special Issue "The Role of Extracellular Matrix in Cancer Development and Progression"
Deadline for manuscript submissions: closed (30 July 2021) | Viewed by 34419
A printed edition of this Special Issue is available here.
Interests: matrix pathobiology; tumor biology; signal transduction; disease markers; molecular targets; proteoglycans; glycosaminoglycans; matrix cell surface receptors; tumorigenesis; inflammation; cytotoxicity
Interests: matrix pathobiology; cancer; inflammation; oxidative stress; cytotoxicity
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The consecutive steps of tumor growth, local invasion, intravasation, extravasation, and invasion of anatomically distant sites, as well as immunosuppression, are obligatorily perpetrated through specific interactions of the tumor cells with their microenvironment. During cancer progression, significant changes can be observed in the properties of extracellular matrices (ECMs) components, which deregulate the behavior of stromal cells, promote tumor-associated angiogenesis and inflammation, and lead to the generation of a tumorigenic microenvironment. Thus, mediators that originate from the ECM have a vital effect on all cellular functions implicated in cancer development and progression. ECM components, including fibrillar proteins, proteoglycans, and glycosaminoglycans, modulate the bioavailability of active mediators, control the stiffness of the stroma immediately correlated to cancer cell invasion, and regulate the metastatic processes and angiogenesis. Various ECM-derived components also have the ability to modulate the immune response and affect the response to therapy and thus need to be taken into account when designing efficient anticancer therapy. Indeed, the ECM effectors regulate processes correlated to chemoresistance, including autophagy and apoptosis.
This Special Issue of Biomolecules entitled “Role of Extracellular Matrix in Development and Cancer Progression” focuses on recent findings in the structural and functional characterization of ECM components and how they relate to the processes involved in the pathogenesis of cancer, and response to therapy. Focusing on the crosstalk between the ECM and cellular processes has helped to identify novel disease markers and therapeutic targets. We invite researchers to submit reviews or regular research articles focusing on this vital crosstalk.
Professor George Tzanakakis
Professor Dragana Nikitovic
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- extracellular matrix
- tumor microenvironment
- fibrillar proteins
- cancer cell functions
- cancer immunobiology
- cancer therapy targets
- hyaluronan in cancer
- epithelial to mesenchymal transition
- metastatic cascade and ECM effectors
- ECM-driven angiogenesis
- matrix metalloproteinases
- matrikines as tumor effectors