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Cells
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Extracellular Matrix-mediated Cancer Cells
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Extracellular Matrix-mediated Cancer Cells

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Motility and Adhesion".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 14387

Special Issue Editors

Dr. Marco Franchi

E-Mail Website
Guest Editor
Department for Life Quality Studies, University of Bologna, 47921 Rimini, Italy
Interests: cancer invasion; extracellular matrix (ECM); epithelial-to-mesenchymal (EMT); 3D cultures; collagen
Special Issues, Collections and Topics in MDPI journals
Dr. Konstantina Kyriakopoulou

E-Mail Website
Guest Editor
“Biochemistry, Biochemical Analysis & Matrix Pathobiology” Res. Group, Laboratory of Biochemistry, Department of Chemistry, University of Patras, 26504 Patras, Greece
Interests: extracellular matrix (ECM); epithelial-to-mesenchymal transition (EMT); cell plasticity; cell morphology; cell signaling

Special Issue Information

Dear Colleagues,

The extracellular matrix (ECM) is ubiquitously present in all connective tissues and represents the first microenvironment that cancer cells from solid tumors must invade to develop intravasation and then metastasis. Many researchers have exclusively focused their investigations on tumor features, but recent studies have demonstrated that tumor development and behavior have to be considered in view of the interactions and crosstalk between cancer cells and the surrounding stromal cells which could remodel a peritumoral ECM favoring cancer cell invasion. Exosomes and microvesicles, tunneling nanotubes, integrins, and signaling are all expressions of such an intense and strategic bidirectional interplay between tumor and ECM. Cancer growth and cancer cell invasion are strongly regulated both by changes of composition and structural array of peritumoral ECM, which can induce epithelial-to-mesenchymal transition (EMT). The aim of this Special Issue is to collect the expertise of international researchers to highlight the roles of intercellular as well as cell–tissue communications involved in cancer cell invasion and metastasis at distant sites.

Prof. Marco Franchi
Dr. Konstantina Kyriakopoulou
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly 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.

Keywords

  • cancer invasion
  • extracellular matrix (ECM)
  • epithelial-to-mesenchymal (EMT)

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Published Papers (2 papers)

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Research

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18 pages, 4665 KiB  
Article
The Heparan Sulfate Proteoglycan Syndecan-1 Triggers Breast Cancer Cell-Induced Coagulability by Induced Expression of Tissue Factor
by Nourhan Hassan, Nico Bückreiß, Janes Efing, Marie Schulz-Fincke, Philipp König, Burkhard Greve, Gerd Bendas and Martin Götte
Cells 2023, 12(6), 910; https://doi.org/10.3390/cells12060910 - 16 Mar 2023
Cited by 6 | Viewed by 3436
Abstract
Syndecan-1 (Sdc-1) upregulation is associated with poor prognosis in breast cancer. Sdc-1 knockdown results in reduced angiogenesis and the dysregulation of tissue factor (TF) pathway constituents. Here, we evaluate the regulatory mechanisms and functional consequences of the Sdc-1/TF-axis using Sdc-1 knockdown and overexpression [...] Read more.
Syndecan-1 (Sdc-1) upregulation is associated with poor prognosis in breast cancer. Sdc-1 knockdown results in reduced angiogenesis and the dysregulation of tissue factor (TF) pathway constituents. Here, we evaluate the regulatory mechanisms and functional consequences of the Sdc-1/TF-axis using Sdc-1 knockdown and overexpression approaches in MCF-7 and MDA-MB-231 breast cancer cells. Gene expression was analyzed by means of qPCR. Thrombin generation and cell migration were detected. Cell-cycle progression and apoptosis were investigated using flow cytometry. In MDA-MB-231 cells, IL6, IL8, VEGF, and IGFR-dependent signaling affected TF pathway expression depending on Sdc-1. Notably, Sdc-1 depletion and TF pathway inhibitor (TFPI) synergistically affected PTEN, MAPK, and STAT3 signaling. At the functional level, the antiproliferative and pro-apoptotic effects of TFPI depended on Sdc-1, whereas Sdc-1’s modulation of cell motility was not affected by TFPI. Sdc-1 overexpression in MCF-7 and MDA-MB-231 cells led to increased TF expression, inducing a procoagulative phenotype, as indicated by the activation of human platelets and increased thrombin formation. A novel understanding of the functional interplay between Sdc-1 and the TF pathway may be compatible with the classical co-receptor role of Sdc-1 in cytokine signaling. This opens up the possibility of a new functional understanding, with Sdc-1 fostering coagulation and platelet communication as the key to the hematogenous metastatic spread of breast cancer cells. Full article
(This article belongs to the Special Issue Extracellular Matrix-mediated Cancer Cells)
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Review

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65 pages, 5901 KiB  
Review
Extracellular Matrix Cues Regulate Mechanosensing and Mechanotransduction of Cancer Cells
by Claudia Tanja Mierke
Cells 2024, 13(1), 96; https://doi.org/10.3390/cells13010096 - 2 Jan 2024
Cited by 37 | Viewed by 10138
Abstract
Extracellular biophysical properties have particular implications for a wide spectrum of cellular behaviors and functions, including growth, motility, differentiation, apoptosis, gene expression, cell–matrix and cell–cell adhesion, and signal transduction including mechanotransduction. Cells not only react to unambiguously mechanical cues from the extracellular matrix [...] Read more.
Extracellular biophysical properties have particular implications for a wide spectrum of cellular behaviors and functions, including growth, motility, differentiation, apoptosis, gene expression, cell–matrix and cell–cell adhesion, and signal transduction including mechanotransduction. Cells not only react to unambiguously mechanical cues from the extracellular matrix (ECM), but can occasionally manipulate the mechanical features of the matrix in parallel with biological characteristics, thus interfering with downstream matrix-based cues in both physiological and pathological processes. Bidirectional interactions between cells and (bio)materials in vitro can alter cell phenotype and mechanotransduction, as well as ECM structure, intentionally or unintentionally. Interactions between cell and matrix mechanics in vivo are of particular importance in a variety of diseases, including primarily cancer. Stiffness values between normal and cancerous tissue can range between 500 Pa (soft) and 48 kPa (stiff), respectively. Even the shear flow can increase from 0.1–1 dyn/cm2 (normal tissue) to 1–10 dyn/cm2 (cancerous tissue). There are currently many new areas of activity in tumor research on various biological length scales, which are highlighted in this review. Moreover, the complexity of interactions between ECM and cancer cells is reduced to common features of different tumors and the characteristics are highlighted to identify the main pathways of interaction. This all contributes to the standardization of mechanotransduction models and approaches, which, ultimately, increases the understanding of the complex interaction. Finally, both the in vitro and in vivo effects of this mechanics–biology pairing have key insights and implications for clinical practice in tumor treatment and, consequently, clinical translation. Full article
(This article belongs to the Special Issue Extracellular Matrix-mediated Cancer Cells)
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