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Cells
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Role of Extracellular Matrix in Cancer and Disease
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Role of Extracellular Matrix in Cancer and Disease

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

Deadline for manuscript submissions: 31 July 2025 | Viewed by 2051

Special Issue Editors

Dr. Maurizio Onisto

E-Mail Website
Guest Editor
Department of Biomedical Sciences, University of Padova, 35100 Padua, Italy
Interests: extra-cellular matrix (ECM) turn-over and remodeling; matrix–metalloproteinases (MMPs) and TIMPs; heparanase; tumor invasiveness and metastasis; epithelial to mesenchymal transition (EMT); SPATA2 (spermatogenesis-associated protein 2)
Special Issues, Collections and Topics in MDPI journals
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. Valentina Masola

E-Mail Website
Guest Editor
Department of Biomedical Sciences, University of Padova, 35100 Padua, Italy
Interests: heparanase; organ fibrosis; inflammation; renal and peritoneal patho-physiology; epithelial to mesenchymal transition (EMT); molecular mechanisms in cancer progression
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The extracellular matrix (ECM) is a complex three-dimensional network composed of proteins, glycoproteins, proteoglycans, and other molecules that provide structural and metabolic support to cells in tissues and organs. The ECM undergoes continuous remodeling by proteases and glycosidases that is strictly controlled under normal conditions and is essential for the maintenance of tissue homeostasis. In pathological situations such as cancer and fibrosis, the remodeling of the ECM is dysregulated and constitutes one of the first events in the progression of the disease. For example, the altered expression of ECM macromolecules in the tumor microenvironment is able to condition the growth, survival and migration of tumor cells themselves. Starting from this evidence, recent studies have focused on identifying new therapeutic and diagnostic strategies targeting ECM molecules. The aim of this Special Issue of Cells is to bring to light new studies that advance our knowledge of the molecular mechanisms involving the ECM in the biogenesis of cancer and other diseases.

Dr. Maurizio Onisto
Dr. Marco Franchi
Dr. Valentina Masola
Guest Editors

Manuscript Submission Information

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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

  • extracellular matrix
  • cancer
  • disease
  • ECM targeting
  • ECM turn-over and remodeling

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Published Papers (4 papers)

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Research

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16 pages, 1545 KiB  
Article
Lidocaine Affects Collagen Breakdown Without Compromising Cell Viability in Cultured Human Tenocytes: An In Vitro Study
by Filippo Randelli, Manuel G. Mazzoleni, Alessandra Menon, Alberto Fioruzzi, Dolaji Henin, Michele Sommariva and Nicoletta Gagliano
Cells 2025, 14(13), 988; https://doi.org/10.3390/cells14130988 - 27 Jun 2025
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Abstract
Local anesthetics (LAs) are frequently administered via peritendinous ultrasound-guided injections for diagnostic and therapeutic purposes. Since in vitro studies have demonstrated LAs’ tenotoxic effects, raising concerns about their safety in infiltrative treatments, and since lidocaine (LD) emerged as one of the most cytotoxic [...] Read more.
Local anesthetics (LAs) are frequently administered via peritendinous ultrasound-guided injections for diagnostic and therapeutic purposes. Since in vitro studies have demonstrated LAs’ tenotoxic effects, raising concerns about their safety in infiltrative treatments, and since lidocaine (LD) emerged as one of the most cytotoxic LAs, we analyzed apoptosis, oxidative stress, and collagen turnover pathways in human tenocytes treated with LD, as well as the possible protection from LD-induced injury elicited by antioxidant ascorbic acid (AA). Tenocytes from gluteal tendons were treated with 0.2 and 1 mg/mL LD, or left untreated (CT), and treated with 50 μg/mL or 250 μg/mL AA. Nuclear morphology, cytochrome c expression, and caspase 3 activation were analyzed to study the effect of LD on apoptosis. Heme Oxygenase 1 (HO-1) mRNA and genes and proteins involved in collagen turnover were investigated using molecular approaches. Our results show that 0.2 and 1 mg/mL LD did not induce apoptosis and did not modify collagen synthesis and maturation. Conversely, increased collagen degradation was observed, and AA was not protective against oxidative stress induction in the presence of LD. Our findings suggest that LD does not affect the cell viability of tenocytes and that peritendinous LD injections are safe in this regard. LD-associated collagen degradation and the AA buffer effect are still debatable. Overall, our study contributes to clarifying the effect of LD on tenocytes’ viability and ECM homeostasis and provides new additional information useful for the safe clinical application of this drug and for further analysis. Full article
(This article belongs to the Special Issue Role of Extracellular Matrix in Cancer and Disease)
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Review

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17 pages, 1258 KiB  
Review
Design and Applications of Extracellular Matrix Scaffolds in Tissue Engineering and Regeneration
by Sylvia Mangani, Marios Vetoulas, Katerina Mineschou, Konstantinos Spanopoulos, Maria dM. Vivanco, Zoi Piperigkou and Nikos K. Karamanos
Cells 2025, 14(14), 1076; https://doi.org/10.3390/cells14141076 - 15 Jul 2025
Abstract
Tissue engineering is a growing field with multidisciplinary players in cell biology, engineering, and medicine, aiming to maintain, restore, or enhance functions of tissues and organs. The extracellular matrix (ECM) plays fundamental roles in tissue development, maintenance, and repair, providing not only structural [...] Read more.
Tissue engineering is a growing field with multidisciplinary players in cell biology, engineering, and medicine, aiming to maintain, restore, or enhance functions of tissues and organs. The extracellular matrix (ECM) plays fundamental roles in tissue development, maintenance, and repair, providing not only structural support, but also critical biochemical and biomechanical cues that regulate cell behavior and signaling. Although its specific composition varies across different tissue types and developmental stages, matrix molecules influence various cell functional properties in every tissue. Given the importance of ECM in morphogenesis, tissue homeostasis, and regeneration, ECM-based bioscaffolds, developed through tissue engineering approaches, have emerged as pivotal tools for recreating the native cellular microenvironment. The aim of this study is to present the main categories of these scaffolds (i.e., natural, synthetic, and hybrid), major fabrication techniques (i.e., tissue decellularization and multidimensional bioprinting), while highlighting the advantages and disadvantages of each category, focusing on biological activity and mechanical performance. Scaffold properties, such as mechanical strength, elasticity, biocompatibility, and biodegradability are essential to their function and integration into host tissues. Applications of ECM-based bioscaffolds span a range of engineering and regenerative strategies, including cartilage, bone, cardiac tissue engineering, and skin wound healing. Despite promising advances, challenges remain in standardization, scalability, and immune response modulation, with future directions directed towards improving ECM-mimetic platforms. Full article
(This article belongs to the Special Issue Role of Extracellular Matrix in Cancer and Disease)
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16 pages, 2105 KiB  
Review
“Unraveling EMILIN-1: A Multifunctional ECM Protein with Tumor-Suppressive Roles” Mechanistic Insights into Cancer Protection Through Signaling Modulation and Lymphangiogenesis Control
by Samanta Muzzin, Enrica Timis, Roberto Doliana, Maurizio Mongiat and Paola Spessotto
Cells 2025, 14(13), 946; https://doi.org/10.3390/cells14130946 - 20 Jun 2025
Viewed by 473
Abstract
EMILIN-1 (Elastin Microfibril Interface Located Protein 1) is an extracellular matrix homotrimeric glycoprotein belonging to the EMILIN/Multimerin family, with both structural and regulatory roles, increasingly recognized for its tumor-suppressive functions. Initially identified for its involvement in elastogenesis and vascular homeostasis, EMILIN-1 has gradually [...] Read more.
EMILIN-1 (Elastin Microfibril Interface Located Protein 1) is an extracellular matrix homotrimeric glycoprotein belonging to the EMILIN/Multimerin family, with both structural and regulatory roles, increasingly recognized for its tumor-suppressive functions. Initially identified for its involvement in elastogenesis and vascular homeostasis, EMILIN-1 has gradually emerged as a key player in cancer biology. It exerts its anti-tumor activity through both direct and indirect mechanisms: by regulating tumor cell proliferation and survival and by modulating lymphangiogenesis and the associated inflammatory microenvironment. At the molecular level, EMILIN-1 inhibits pro-oncogenic signaling pathways, such as ERK/AKT and TGF-β, via its selective interaction with α4/α9 integrins. In the tumor microenvironment, it contributes to tissue homeostasis by restraining aberrant lymphatic vessel formation, a process closely linked to tumor dissemination and immune modulation. Notably, EMILIN-1 expression is frequently reduced or its structure altered by proteolytic degradation in advanced cancers, correlating with disease progression and poor prognosis. This review summarizes the current knowledge on EMILIN-1 in cancer, focusing on its dual function as an active extracellular matrix regulator of intercellular signaling. Particular attention is given to its mechanistic role in the control of cell proliferation, underscoring its potential as a novel biomarker and therapeutic target in oncology. Full article
(This article belongs to the Special Issue Role of Extracellular Matrix in Cancer and Disease)
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51 pages, 1586 KiB  
Review
ECM Mechanics Control Jamming-to-Unjamming Transition of Cancer Cells
by Claudia Tanja Mierke
Cells 2025, 14(13), 943; https://doi.org/10.3390/cells14130943 - 20 Jun 2025
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Abstract
Cancer metastasis constitutes a multifactorial phenomenon that continues to confound therapeutic strategies. The biochemical signals governing motile phenotypes have been extensively characterized, but mechanobiological interactions have only recently been integrated into cancer cell motility models and remain less well elucidated. The identification of [...] Read more.
Cancer metastasis constitutes a multifactorial phenomenon that continues to confound therapeutic strategies. The biochemical signals governing motile phenotypes have been extensively characterized, but mechanobiological interactions have only recently been integrated into cancer cell motility models and remain less well elucidated. The identification of the biochemically and mechanically controlled epithelial–mesenchymal transition (EMT) of cancer cells, which occurs either completely or partially, has led to a major breakthrough and a universal phenomenon in cancers. In addition, a relatively new theory based on mechanobiological aspects called “jamming-to-unjamming transition” is being proposed to explain the transition of cancer cells to an invasive phenotype. The latter transition may help to better understand the different types of 3D migration and invasion of cancer cells. Similarly to EMT, the transition from jamming to unjamming seems to be controlled by molecular and physical factors, including cell mechanics and mechanical cues from the extracellular matrix (ECM) of the tumor microenvironment (TME). It is challenging to grasp the distinctions between the transition from jamming to unjamming and EMT, as they appear to be the same at first glance. However, upon closer examination, the two transitions are quite separate. Moreover, it is still unclear whether both transitions may act synergistically. This review highlights the most important breakthroughs in the transition from jamming to unjamming, with a focus on mechanobiology and extracellular environmental aspects, and it compares them with those of EMT. In addition, the impact of the TME, such as ECM scaffold and cancer-associated fibroblasts (CAFs) on the jamming-to-unjamming transition is discussed. Finally, the research frontiers and future directions in the field of mechanobiological research in cancer metastasis are outlined. Full article
(This article belongs to the Special Issue Role of Extracellular Matrix in Cancer and Disease)
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