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Cancers
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Extracellular Matrix Proteins in Cancer
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Extracellular Matrix Proteins in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 5030

Special Issue Editors

Dr. Dragana Nikitovic

E-Mail Website
Guest Editor
Laboratory of Histology-Embryology, School of Medicine, The University of Crete, 71003 Heraklion, Greece
Interests: matrix pathobiology; cancer; inflammation; oxidative stress; cytotoxicity; matrix pathobiology
Special Issues, Collections and Topics in MDPI journals
Dr. Aikaterini Berdiaki

E-Mail Website
Guest Editor
Laboratory of Histology-Embryology, Medical School, University of Crete, 71003 Heraklion, Greece
Interests: histology; cytology; tumor microenvironment

Special Issue Information

Dear Colleagues,

The transformed extracellular matrix (ECM) constitutes the non-cellular component of a cancerous microenvironment, and its interactions with cellular components (tumor cells, normal tissue cells, blood vessels, stromal cells and cells of the immune system) modulate cell function and morphology, signaling transductions and subsequently tumor development. Protein ECM components include proteoglycans (extracellular, pericellular/basement membrane and cell surface PGs), fibrous proteins (collagens, elastin) and glycoproteins (laminin, fibronectin). ECM remodeling and changes in composition influence cell proliferation, motility, adhesion and invasion.

This Special Issue focuses on describing and updating the role of ECM proteins in different cancer-type microenvironments as well as defining ECM-associated molecular and structural mechanisms in tumor development.

Original research articles and review articles related to the topic are invited for this Special Issue.

We look forward to receiving your contributions.

Dr. Dragana Nikitovic
Dr. Aikaterini Berdiaki
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 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. 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
  • tumor microenvironment
  • ECM proteins
  • proteoglycans
  • glycoproteins
  • collagens
  • fibrous proteins
  • molecular mechanisms

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Published Papers (4 papers)

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Research

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28 pages, 15072 KiB  
Article
Unravelling Paclitaxel Resistance in Gastric Cancer: The Role of Small Extracellular Vesicles in Epithelial Mesenchymal Transition and Extracellular Matrix Remodelling
by Giorgia Panzetta, Annalisa Schirizzi, Francesco Balestra, Maria De Luca, Nicoletta Depalo, Federica Rizzi, Angela Dalia Ricci, Giampiero De Leonardis, Claudio Lotesoriere, Gianluigi Giannelli, Rosalba D’Alessandro and Maria Principia Scavo
Cancers 2025, 17(8), 1360; https://doi.org/10.3390/cancers17081360 - 18 Apr 2025
Viewed by 466
Abstract
Background: Gastric cancer (GC) is a highly aggressive disease often complicated by resistance to chemotherapy agents like paclitaxel (PTX), which targets microtubules to induce apoptosis. Resistance arises through complex molecular mechanisms, including the overexpression of pro-angiogenic factors (VEGFA, ANG-2), activation of survival pathways [...] Read more.
Background: Gastric cancer (GC) is a highly aggressive disease often complicated by resistance to chemotherapy agents like paclitaxel (PTX), which targets microtubules to induce apoptosis. Resistance arises through complex molecular mechanisms, including the overexpression of pro-angiogenic factors (VEGFA, ANG-2), activation of survival pathways (PDGFRβ, PPARγ), and epithelial-mesenchymal transition (EMT) driven by proteins such as VIM, E-CAD, N-CAD, and FLOT-1. The extracellular matrix (ECM), regulated by COL1A1 and influenced by PPARγ, acts as a physical barrier to drug penetration. Small extracellular vesicles (sEVs) have emerged as critical mediators of intercellular communication and may influence these resistance pathways. Methods: This study investigated the role of sEVs isolated from metastatic GC patients treated with Ramucirumab and PTX. Patients were stratified by progression-free survival (PFS) into rapidly progressing (RP) and controlled disease (CD) groups. sEVs from these patients were applied to HCEC-1CT and HEPA-RG cell lines. Cell viability assays, gene and protein expression analyses, and bioinformatic studies were conducted to assess the impact of sEVs on resistance-related markers. Results: Results showed that sEVs from CD patients reduced the expression of markers associated with drug resistance, while sEVs from RP patients increased these markers, promoting angiogenesis, EMT, and ECM remodeling. These changes correlated with enhanced cell survival and resistance phenotypes. Bioinformatic analyses confirmed that sEVs modulate inflammation, ECM dynamics, and EMT pathways. Conclusions: In conclusion, sEVs from metastatic GC patients significantly influence chemoresistance and tumor progression. Targeting sEV-mediated signaling may offer novel therapeutic strategies to overcome resistance and improve treatment outcomes in gastric cancer. Full article
(This article belongs to the Special Issue Extracellular Matrix Proteins in Cancer)
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18 pages, 2615 KiB  
Article
The Vimentin-Targeting Drug ALD-R491 Partially Reverts the Epithelial-to-Mesenchymal Transition and Vimentin Interactome of Lung Cancer Cells
by Marieke Rosier, Anja Krstulović, Hyejeong Rosemary Kim, Nihardeep Kaur, Erhumuoghene Mary Enakireru, Deebie Symmes, Katalin Dobra, Ruihuan Chen, Caroline A. Evans and Annica K. B. Gad
Cancers 2025, 17(1), 81; https://doi.org/10.3390/cancers17010081 - 30 Dec 2024
Viewed by 1324
Abstract
Background: The epithelial-to-mesenchymal transition (EMT) is a common feature in early cancer invasion. Increased vimentin is a canonical marker of the EMT; however, the role of vimentin in EMT remains unknown. Methods: To clarify this, we induced EMT in lung cancer cells with [...] Read more.
Background: The epithelial-to-mesenchymal transition (EMT) is a common feature in early cancer invasion. Increased vimentin is a canonical marker of the EMT; however, the role of vimentin in EMT remains unknown. Methods: To clarify this, we induced EMT in lung cancer cells with TGF-β1, followed by treatment with the vimentin-targeting drug ALD-R491, live-cell imaging, and quantitative proteomics. Results: We identified 838 proteins in the intermediate filament fraction of cells. TGF-β1 treatment increased the proportion of vimentin in this fraction and the levels of 24 proteins. Variants of fibronectin showed the most pronounced increase (137-fold), followed by regulators of the cytoskeleton, cell motility, and division, such as the mRNA-splicing protein SON. TGF-β1 increased cell spreading and cell migration speed, and changed a positive correlation between cell migration speed and persistence to negative. ALD-R491 reversed these mesenchymal phenotypes to epithelial and the binding of RNA-binding proteins, including SON. Conclusions: These findings present many new interactors of intermediate filaments, describe how EMT and vimentin filament dynamics influence the intermediate filament interactome, and present ALD-R491 as a possible EMT-inhibitor. The observations support the hypothesis that the dynamic turnover of vimentin filaments and their interacting proteins govern mesenchymal cell migration, EMT, cell invasion, and cancer metastasis. Full article
(This article belongs to the Special Issue Extracellular Matrix Proteins in Cancer)
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Review

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20 pages, 1081 KiB  
Review
Implication of the Extracellular Matrix in Metastatic Tumor Cell Dormancy
by Chloe Redoute-Timonnier and Patrick Auguste
Cancers 2024, 16(23), 4076; https://doi.org/10.3390/cancers16234076 - 5 Dec 2024
Cited by 1 | Viewed by 1239
Abstract
Metastasis is the main cause of cancer-related deaths. The formation and growth of metastasis is a multistep process. Tumor cells extravasating in the secondary organ are in contact with a new microenvironment and a new extracellular matrix (ECM), called the metastatic niche. Some [...] Read more.
Metastasis is the main cause of cancer-related deaths. The formation and growth of metastasis is a multistep process. Tumor cells extravasating in the secondary organ are in contact with a new microenvironment and a new extracellular matrix (ECM), called the metastatic niche. Some components of the ECM, such as periostin, can induce tumor cell growth in macrometastasis. In contrast, other components, such as Thrombospondin 1 (TSP-1), can maintain isolated cells in a dormant state. During dormancy, intracellular signaling activation, such as p38, maintains tumor cells arrested in the cell-cycle G0 phase for years. At any moment, stress can induce ECM modifications and binding to their specific receptors (mainly integrins) and reactivate dormant tumor cell growth in macrometastasis. In this review, we describe the tumor microenvironment of the different niches implicated in tumor cell dormancy. The role of ECM components and their associated receptors and intracellular signaling in the reactivation of dormant tumor cells in macrometastasis will be emphasized. We also present the different methodologies and experimental approaches used to study tumor cell dormancy. Finally, we discuss the current and future treatment strategies to avoid late metastasis relapse in patients. Full article
(This article belongs to the Special Issue Extracellular Matrix Proteins in Cancer)
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17 pages, 1015 KiB  
Review
The Role of eHsp90 in Extracellular Matrix Remodeling, Tumor Invasiveness, and Metastasis
by Pragya Singh and Daniel G. Jay
Cancers 2024, 16(22), 3873; https://doi.org/10.3390/cancers16223873 - 19 Nov 2024
Cited by 1 | Viewed by 1450
Abstract
Identifying proteins that act in tumor invasiveness and metastasis remains a critical unmet need in our search for effective cancer therapy. Hsp90, an abundant intracellular chaperone protein, plays a key role in maintaining cell homeostasis, and its elevated activity is pivotal in cancer [...] Read more.
Identifying proteins that act in tumor invasiveness and metastasis remains a critical unmet need in our search for effective cancer therapy. Hsp90, an abundant intracellular chaperone protein, plays a key role in maintaining cell homeostasis, and its elevated activity is pivotal in cancer progression. Due to the reliance of cancer cells on Hsp90’s chaperone function to sustain tumor growth and spread, Hsp90 inhibitors have been the subject of numerous clinical trials over the past two decades. However, these efforts have largely been unsuccessful, primarily due to the cellular toxicity caused by pan-Hsp90 inhibitors at doses required for anticancer efficacy. Therefore, novel approaches to target Hsp90 are necessary. An identified subpopulation of Hsp90 located outside cells (eHsp90) may offer a promising alternative as a therapeutic target against cancer. Studies including our own have shown that eHsp90 is released specifically by cancer cells, and eHsp90 has unique interactors and functions extracellularly to promote tumor invasiveness, the initial step in metastasis. Inhibition of eHsp90 has been shown to suppress metastasis in animal models, indicating its therapeutic potential, although the underlying mechanisms remain incompletely understood. Cancer cells modulate the tumor microenvironment (TME) during the invasion, especially the ECM proteins and the state of the ECM is a strong predictor of invasive and metastatic cancer. Given that most of the known eHsp90 clients are ECM proteins or are proteins involved in ECM modulation, ECM remodelling could be the key mechanism through which eHsp90 enhances invasiveness. This review will focus on ECM modulation by eHsp90 as a driver of cancer invasion and metastasis. We will also discuss the potency of inhibiting eHsp90 in inhibiting invasion and metastatic spread in preclinical models and the using circulating Hsp90 patient samples as a biomarker of cancer invasion and metastasis. Full article
(This article belongs to the Special Issue Extracellular Matrix Proteins in Cancer)
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