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Cancers
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Decoding the Dynamic Matrix Complexity in Cancer
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Decoding the Dynamic Matrix Complexity in Cancer

A Special Issue of Cancers (ISSN 2072-6694) belonging to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 4218

Editors

Prof. Dr. Nikos Karamanos

E-Mail Website
Guest Editor
Biochemistry, Biochemical Analysis and Matrix Pathobiology Research Group, Laboratory of Biochemistry, Department of Chemistry, University of Patras, 26504 Patras, Greece
Interests: matrix pathobiology; molecular mechanisms in cancer progression; proteoglycans; glycosaminoglycans; metalloproteinases; growth factors; tumor microenvironment; 3D cell culture models
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Zoi Piperigkou

E-Mail Website
Guest Editor
Biochemistry, Biochemical Analysis and Matrix Pathobiology Research Group, Laboratory of Biochemistry, Department of Chemistry, University of Patras, 26504 Patras, Greece
Interests: extracellular matrix targeting; 3D cell culture models; cell signaling; estrogen receptors; proteoglycans; tumor microenvironment; microRNAs; epigenetics; bioscaffolds
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Luisa Bracci

E-Mail Website
Guest Editor
Biochemistry and Molecular Mechanisms of Cancer Research Group, U&E PreMed Laboratory, Department of Medical Biotechnologies, University of Siena, 53100 Siena, Italy
Interests: proteoglycans; glycosaminoglycans; cell migration; metastasis; cancer ECM; tumor markers; synthetic peptides

Special Issue Information

Dear Colleagues,

Extracellular matrices (ECMs) are highly dynamic three-dimensional (3D) structural and cell regulatory meshworks of macromolecules, such as proteoglycans/glycosaminoglycans (PGs/GAGs), collagens, laminins, elastin, (glyco)proteins, and matrix-degrading enzymes. Matrix macromolecules are characterized by high structural complexity and heterogeneity. They form complex networks through which they dynamically communicate with cells and shape the complex tumor microenvironment. ECMs are not merely structural components, but rather active and critical regulators of several homeostatic and pathological processes, such as cancer. Their molecular composition varies among different tissues and undergoes significant modifications and remodeling during cancer progression. The elucidation of the mechanistic aspects governing matrix assembly and modifications, as well as cell–cell and cell–matrix interactions, is of critical importance to fully understand cancer pathobiology and to identify tumor biomarkers and novel therapeutic targets. Moreover, 3D cell culture models and bioscaffolds that mimic native ECM architecture and biophysical properties have emerged as powerful tools to investigate cell–matrix crosstalk and the dynamic interactions within the tumor microenvironment. This Special Issue of Cancers seeks to highlight the roles of effective matrix macromolecules, including matrix remodeling enzymes, PGs/GAGs, specific types of collagens and matrix (glyco)proteins, the modeling of tumor microenvironment complexity as well as the mechanisms underlying the dynamic cancer-associated cell–matrix interactions that drive cancer development and aggressiveness.

We invite submissions of original research articles and reviews that address topics that include but are not limited to the following, which are aligned with the aim of decoding dynamic matrix complexity:

  • Proteoglycans and Glycosaminoglycans as Dynamic Regulators of Tumor Plasticity
  • Targeting Matrix Remodeling Enzymes in Cancer Progression
  • Collagen and Glycoprotein Networks as Biomarkers and Therapeutic Targets
  • Cell Surface Matrix Receptors and Effectors in Pre-metastatic Niche Formation
  • Matrix-Derived Bioscaffolds for Modeling Tumor Microenvironment Complexity
  • 3D Cell Culture Models in Mimicking Tumor Microenvironment

Should you have any questions, require further information, or need any assistance, please do not hesitate to reach out to us. We are happy to support and facilitate your participation.

Thank you for your interest in this Special Issue. We look forward to your contributions.

Prof. Dr. Nikos Karamanos
Prof. Dr. Zoi Piperigkou
Prof. Dr. Luisa Bracci
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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers 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 2900 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

  • extracellular matrix
  • cancer pathobiology
  • 3D spheroids/organoids
  • modeling tumor microenvironment complexity
  • matrix-based bioscaffolds
  • matrix remodeling
  • cell surface matrix mediators and effectors
  • matrix degrading enzymes
  • proteoglycans/glycosaminoglycans
  • collagen
  • matrix (glyco)proteins
  • molecular targeting

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Published Papers (3 papers)

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Research

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26 pages, 6376 KB  
Article
Large Extracellular Vesicle-Derived Latent MMP-8 and Gelatinolytically Active MMP-2 as Potential Circulating Markers for Lymph Node Metastasis in Breast Cancer
by Liali Yousef Talat, Amr Ahmed WalyEldeen, Ghada Mohamed, Maher H. Ibraheem, Maysaa Mahmoud Maher, Sherif Abdelaziz Ibrahim, Hebatallah Hassan and Martin Götte
Cancers 2026, 18(9), 1464; https://doi.org/10.3390/cancers18091464 - 2 May 2026
Viewed by 2764
Abstract
Background: Lymph node metastasis (LNM) is a determinant of prognosis and in guiding chemotherapy decisions in breast cancer. Herein, we aimed to discover the protease content of the circulating large extracellular vesicles (L-EVs) as potential markers for LNM. Methods: L-EVs were isolated from [...] Read more.
Background: Lymph node metastasis (LNM) is a determinant of prognosis and in guiding chemotherapy decisions in breast cancer. Herein, we aimed to discover the protease content of the circulating large extracellular vesicles (L-EVs) as potential markers for LNM. Methods: L-EVs were isolated from the plasma of chemotherapy-naïve breast cancer patients with negative LNM (nLNM, n = 40) and positive LNM (pLNM, n = 32) patients using differential centrifugation. The isolated L-EVs were characterized by Transmission Electron Microscopy, dynamic light scattering and EV marker profiling, and their protease content was profiled using unbiased proteome profiler human protease array. Results: Protease profiling uncovered that L-EVs contained significantly elevated levels of MMP-8 (p < 0.001) and MMP-9 (p < 0.05) in pLNM versus nLNM patients. Further validation by Western blotting confirmed that latent MMP-8 was significantly increased (p < 0.01) in L-EVs from pLNM patients. Interestingly, zymography revealed that L-EVs isolated from pLNM patients contained higher levels of latent MMP-9 compared with those from nLNM patients, whereas gelatinolytically active MMP-2 was only detected in L-EVs from pLNM patients and not in those from nLNM. Online datasets revealed that higher MMP-8 and MMP-9 mRNA levels were associated with poorer overall, relapse-free, and distant metastasis-free survival. Receiver operating characteristic (ROC) plotter analyses indicated that MMP-2 and MMP-8 may serve as predictive biomarkers for response to specific chemotherapeutic regimens. Conclusions: These findings highlight the potential clinical utility of L-EV-derived MMP-2, MMP-8, and MMP-9 expressions and/or activities, as non-invasive blood-based markers associated with nodal progression and therapeutic response. Full article
(This article belongs to the Special Issue Decoding the Dynamic Matrix Complexity in Cancer)
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Review

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35 pages, 8548 KB  
Review
Proteoglycans as Regulators of Receptor Trafficking and Spatial Signaling in Cancer
by Aikaterini Berdiaki, Maria Konstantaraki, Zuha Ajlan, Maria Marmara, Aristidis Tsatsakis, George Tzanakakis and Dragana Nikitovic
Cancers 2026, 18(17), 2832; https://doi.org/10.3390/cancers18172832 - 1 Sep 2026
Abstract
Cellular responses depend on the coordinated regulation of receptor activation, trafficking, and signaling across distinct membrane and intracellular compartments. Proteoglycans (PGs), traditionally regarded as structural components of the extracellular matrix and co-receptors, are now emerging as active organizers of receptor dynamics. This review [...] Read more.
Cellular responses depend on the coordinated regulation of receptor activation, trafficking, and signaling across distinct membrane and intracellular compartments. Proteoglycans (PGs), traditionally regarded as structural components of the extracellular matrix and co-receptors, are now emerging as active organizers of receptor dynamics. This review examines the mechanisms through which PGs regulate receptor trafficking and spatial signaling in cancer. Recent studies addressing the roles of proteoglycans in receptor clustering, endocytic pathway selection, intracellular trafficking, recycling, lysosomal degradation, endosomal signaling, exosome biogenesis, and nuclear receptor transport were evaluated, with particular attention to the strength of direct evidence for trafficking. Particular attention was given to the complementary functions of proteoglycan core proteins, glycosaminoglycan chains, and extracellular matrix remodeling in shaping receptor behavior. Current evidence demonstrates that proteoglycans govern multiple stages of receptor biology by controlling ligand presentation, receptor accessibility, membrane organization, intracellular trafficking, and signaling persistence. Individual proteoglycans exert distinct effects on receptor fate, ranging from receptor downregulation and degradation to sustained endosomal signaling and nuclear receptor translocation. Cancer-associated alterations in proteoglycan expression, glycosaminoglycan sulfation, heparanase activity, ectodomain shedding, and glycocalyx organization remodel signaling networks, strengthen communication between tumor and stromal cells, and promote tumor progression, immune modulation, metastasis, and therapeutic resistance. Proteoglycans have emerged as fundamental regulators of receptor trafficking and signaling architecture. Through the integration of extracellular matrix organization with receptor dynamics, they shape the spatial and temporal properties of oncogenic signaling. This conceptual framework broadens our understanding of tumor biology and identifies proteoglycan-dependent regulation of receptor trafficking as a promising avenue for future therapeutic intervention. Full article
(This article belongs to the Special Issue Decoding the Dynamic Matrix Complexity in Cancer)
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23 pages, 1010 KB  
Review
Decoding Post-Transcriptional Networks Governing the Melanoma Extracellular Matrix
by Elias N. Katsoulieris, Paraskevi Ioannou and Nikolaos A. Afratis
Cancers 2026, 18(14), 2326; https://doi.org/10.3390/cancers18142326 - 18 Jul 2026
Viewed by 396
Abstract
The extracellular matrix (ECM) is a key determinant of melanoma progression, regulating tumor cell behavior through biochemical and biomechanical cues. MicroRNAs (miRNAs) have emerged as critical post-transcriptional regulators of gene expression and are increasingly recognized as important modulators of ECM remodeling in cancer. [...] Read more.
The extracellular matrix (ECM) is a key determinant of melanoma progression, regulating tumor cell behavior through biochemical and biomechanical cues. MicroRNAs (miRNAs) have emerged as critical post-transcriptional regulators of gene expression and are increasingly recognized as important modulators of ECM remodeling in cancer. This review summarizes current evidence on miRNA-mediated regulation of ECM components and ECM-associated pathways in melanoma (matrix-miRNAs). We examine studies reporting miRNAs that directly target structural ECM molecules such as collagens, laminins, fibronectin, hyaluronan-related enzymes, and proteoglycans, as well as miRNAs that indirectly regulate ECM dynamics through modulation of matrix metalloproteinases, signaling pathways, and transcription factors. The collected evidence indicates that miRNAs form complex regulatory networks that influence tumor proliferation, invasion, metastasis, angiogenesis, immune evasion, and therapy resistance by reshaping the tumor microenvironment. Tumor-suppressive miRNAs generally inhibit ECM remodeling and metastatic behavior, whereas oncogenic miRNAs promote matrix degradation and a pro-invasive microenvironment. Importantly, many miRNAs exert pleiotropic effects by targeting multiple components of interconnected signaling pathways, resulting in context-dependent outcomes during melanoma progression. Overall, miRNA-dependent regulation of the ECM represents a crucial layer of control in melanoma biology. Understanding these regulatory circuits may provide novel opportunities for biomarker development and therapeutic intervention targeting both tumor cells and their surrounding microenvironment. Full article
(This article belongs to the Special Issue Decoding the Dynamic Matrix Complexity in Cancer)
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