Matrix metalloproteinases (MMPs) are key enzymes involved in extracellular matrix (ECM) remodeling, regulating a wide range of cellular and immune processes in both homeostatic and pathological conditions. Host–microbiota interactions play a critical role in maintaining ECM balance; however, during dysbiosis, this regulation is disrupted, leading to compromised barrier integrity, pathogen translocation into circulation, and the development of systemic diseases and cancer. This review highlights the bidirectional relationship between MMP expression/activity and microbiota dysbiosis, emphasizing tissue-specific alterations in MMP activity that contribute to disease progression. In addition, it integrates interdisciplinary evidence to illustrate the MMP-dependent mechanisms underlying various pathologies associated with oral and gut microbiome dysbiosis, including long-range effects through the gut–skin and gut–brain axes. Thus, this review introduces the emerging field of MatrixBiome, which explores the complex interactions between the ECM, microbiota, and host tissues. Finally, it also outlines therapeutic strategies to modulate MMP levels, either indirectly through microbiome-targeted approaches (e.g., prebiotics, probiotics, and postbiotics) or directly using MMP inhibitors, offering promising avenues for future clinical interventions.

The integration of semi-transparent photovoltaics into the roof of greenhouses is an emerging technique used in recent years, due to the simultaneous energy and food production from the same piece of land. Although shading in many cases is a solution to maintain the desired microclimate, in the case of photovoltaic installations, the permanent shading of the crop is a challenge, due to the importance of light to the growth, morphogenesis, and other critical physiological processes. In this study, the effect of shade from semi-transparent photovoltaics on a strawberry crop (Fragaria x ananassa Duch.) was examined, in terms of growth and quality (phenolic and flavonoid concentration of fruits). According to the results, in non-shaded plants, there was a trend of larger plants, but without a significant change in leaf number, while the total number of flowers was slightly higher at the end of the cultivation period. Moreover, it was found that the percentage change between the number of ripe fruits was smaller than that of the corresponding change in fruit weight, implying the increased size of the fruits in non-shaded plants. Finally, regarding the antioxidant capacity, it was clearly demonstrated that shading increased the total phenolic content, as well as the free-radical-scavenging activity of the harvested fruits. Although the shading from the semi-transparent photovoltaics did not assist the production of large fruits, it did not affect their number and increased some of their quality characteristics. In addition, the advantageous impact of the semi-transparent photovoltaics in the energy part must not be neglected.

Background: Breast cancer, one of the most researched cancers in oncology, remains the primary cause of cancer-related mortality in women. Its biological complexity, which includes phenotypic, genetic, and microenvironmental aspects, makes modeling and treatment quite difficult. The need for more physiologically realistic models is highlighted by the comparison of two-dimensional (2D) cell cultures with 3D breast-cancer-derived spheroids, which discloses how important pathways such as epidermal growth factor receptor (EGFR) and insulin-like growth factor I receptor (IGF-IR) influence cell behavior and extracellular matrix (ECM) macromolecular expression. Methods: The purpose of this study was to utilize novel 3D cell platforms to assess the effect of inhibiting the EGFR and IGF-IR pathways, alone or in combination, on the functional properties and the expression levels of certain matrix metalloproteinases (MMPs) which are implicated in breast cancer progression (i.e., triple-negative and luminal A breast cancer subtypes) and related with the EGFR and IGF-ΙR molecular network, as also demonstrated through STRING analysis. Results: Our results demonstrated potential crosstalk between EGFR and IGF-IR signaling, which influences cell proliferation and spheroid growth, dissemination, and migration. Significant phenotypic changes proposed between 2D and 3D cell cultures, and alterations in the expression of MMPs, were also recorded. Conclusions: Both breast cancer cell lines retained acknowledged characteristics across the tested models while also exhibiting new, condition-dependent properties. Overall, our findings enhance our understanding on the interplay between the EGFR and IGF-IR pathways and underscore the value of 3D models in revealing key biological processes underlying distinct breast cancer phenotypes.

Extracellular matrix (ECM) and its dynamic remodeling contribute to the progression of breast cancer, the most prevailing cancer type in women. Glypicans (GPCs) function as cell co‐receptors by facilitating the formation of ligand–receptor complexes. An important regulator in the context of breast cancer progression is the JAK/STAT signaling pathway that oversees the expression of genes associated with cancer cell characteristics. Epidermal growth factor receptor (EGFR) is a pivotal player in this process. The aim of this study is to examine the effect of the EGFR and JAK/STAT signaling pathways on GPCs expression in breast cancer cells with different estrogen receptor (ER) status, depicting different breast cancer subtypes. To this end, the ERα‐positive MCF‐7, and the ERβ‐positive MDA‐MB‐231 breast cancer cell lines were evaluated in terms of the impact of downstream inhibition of both pathways on the functional properties as well as the expression of GPCs 1‐6 genes. Notably, the downstream inhibition of both EGFR and JAK/STAT cascades mitigate cell proliferation and migration, while increasing cell adhesion on collagen type I in an ER‐independent manner. However, the inhibition exhibited a cell‐line‐dependent effect on GPC expression, as in MCF‐7 cells GPCs expression is mostly downregulated excepting GPC‐4 and GPC‐5. Conversely, in MDA‐MB‐231 cells, EGFR and JAK/STAT activation is essential for maintaining GPCs at low levels. Additionally, STRING analysis identified the small leucine‐rich PG decorin as a putative link between all GPCs and EGFR. Subsequently, a deeper understanding on the effect of EGFR and JAK/STAT signaling may shed light into the role and interplay between GPCs and decorin in breast cancer progression, thus contributing to novel therapeutic solutions.

Marine invertebrates, particularly Holothurians, have emerged as valuable sources of bioactive compounds with potential anticancer properties. In this study, we investigated the effects of two acidic polysaccharide-enriched (APs) fractions (Ht1 and Ht2) from the sea cucumber species Holothuria tubulosa on the highly invasive cell line MDA-MB-231. Functional assays were performed to assess cell viability, migratory potential, adhesion on collagen I, and cell morphology, alongside gene expression analysis. Additionally, a preliminary evaluation of their effects on three-dimensional breast cancer cell-derived spheroids was conducted. Both AP fractions exerted anticancer effects by decreasing cell viability. Ht1 showed a significant inhibitory effect on cell migration, increased adhesion on collagen I, and exhibited a trend to transform the mesenchymal MDA-MB-231 cells to a more epithelial phenotype. Treatment with the AP fractions modulated the expression of genes, such as the epithelial marker E-cadherin (for the Ht1), a key cell adhesion molecule, and the matrix metalloproteinases 7 and 9 (for the Ht2), enzymes involved in extracellular matrix remodeling, which hold critical roles in cancer progression and metastasis. No significant effects were observed on spheroids, possibly due to the high charge and hydrophilicity of the APs, leading to poor penetration into the inner spheroid layers. Although preliminary, these findings highlight the potential of H. tubulosa-derived APs as promising antineoplastic agents, warranting further investigation into their mechanisms of action and structural characterization.

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.