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Αγαπητές/οί,
Στη δεύτερη ομάδα σεμιναρίων προόδου εαρινού εξαμήνου θα παρουσιάσουν τα σεμινάρια οι: Κ.Π. Ξαρχάκος, Σ. Μαυράκη, Μ. Ζώτο, Ι. Αθανασοπούλου και Σ. Μπλάνα.
Οι παρουσιάσεις θα γίνουν την Πέμπτη, 2/7, στο χρονικό διάστημα 10.00 -
12.30 στο σύνδεσμο
https://upatras-gr.zoom.us/j/92702932162?pwd=oo2u933CgpbJ8SdUGVXkhyXLuLRGfj.1.
Για περισσότερες λεπτομέρειες, δείτε παρακαλώ τα επισυναπτόμενα αρχεία.
Με εκτίμηση,
Δ. Βύνιος
Abstract Seminar, Athanasopoulou
Name: Dimitrios-Ilias Zafeirakopoulos
Title: Effect of serglycin suppression on proteostasis mechanisms in
multiple myeloma cells
Supervisor: Achilleas D. Theocharis, Professor
Date: 12 June 2026
Time: 10:00 AM
Link: https://upatras-gr.zoom.us/j/92702932162?pwd=oo2u933CgpbJ8SdUGVXkhyXLuLRGfj.1
Abstract
In malignancies, such as multiple myeloma (MM), aberrant expression of proteoglycans (PGs) and other extracellular matrix (ECM) macromolecules is observed, thus promoting ECM remodeling. The ECM serves as a three-dimensional network critical for tissue structure and cellular functions. Serglycin (SRGN), the only known intracellular PG, was initially characterized for its role in the maturation of secretory granules and the regulation of cargo bioavailability in the ECM. Recent data have identified SRGN as a multifunctional regulator of oncogenic signaling and tumor cell phenotype. Previous studies from our laboratory demonstrated a correlation between increased SRGN expression and enhanced tumor aggressiveness across several malignancies.
In multiple myeloma (MM), SRGN influences cell survival and disease progression by interacting with components of the bone marrow microenvironment, thereby constituting a potential biomarker and therapeutic target. Elevated levels of unfolded proteins in the endoplasmic reticulum (ER) lumen are a common feature of malignant cells, a phenomenon known as ER stress. To cope with ER stress, the unfolded protein response (UPR) pathway is activated, which is mediated by PERK, IRE1α, and ATF6, aiming to restore proteostasis through adaptive responses, such as protein folding and synthesis regulation. However, if these mechanisms fail and the stress is prolonged, the UPR shifts towards a terminal state that triggers apoptosis. In parallel with the UPR, the ubiquitin-proteasome system (UPS), responsible for removing misfolded or damaged proteins, is also activated. Together, they support cancer cell survival, proliferation, and therapy resistance. Targeting UPS or UPR components can disrupt proteostasis in tumors, offering promising therapeutic strategies.
The aim of the present work is to investigate the role of SRGN and UPR status in MM cell lines U266 and H929, both of which express high levels of SRGN and UPR markers. We observed that H929 cells maintain elevated levels of active UPR compared to U266 cells and exhibit rapid proliferation capacity. Both MM cell lines utilized UPR as a survival mechanism, as shown by the loss of viability induced by inhibiting each UPR branch. SRGN expression was silenced using siRNA, and the effects on key components of the UPR and UPS were assessed. SRGN silencing caused disruption of pro-survival UPR in both MM cell lines, accompanied by partial loss of cell viability. Simultaneously, SRGN depletion stimulated caspase-dependent apoptosis and induction of apoptotic UPR markers expression, pinpointing its tumorigenic aspect in MM.
Name: Aikaterini-Eleftheria Mineschou
Title: Elastin-Derived Peptides (EDPs) Orchestrate Cancer Cell Plasticity and Molecular Dynamics across 2D and 3D cell models
Supervisor: Nikos K. Karamanos, Professor
Date: 15 June 2026
Time: 11:00 am
Zoom link: https://upatras-gr.zoom.us/j/92702932162?pwd=oo2u933CgpbJ8SdUGVXkhyXLuLRGfj.1
ABSTRACT: BREAST CANCER IS ONE OF THE MOST COMMON AND HETEROGENEOUS MALIGNANCIES AFFECTING WOMEN WORLDWIDE AND REMAINS A LEADING CAUSE OF CANCER-RELATED MORTALITY. IN ADDITION TO GENETIC AND MOLECULAR ALTERATIONS WITHIN TUMOR CELLS, CANCER PROGRESSION IS STRONGLY INFLUENCED BY THE TUMOR MICROENVIRONMENT (TME), PARTICULARLY THE EXTRACELLULAR MATRIX (ECM). THE ECM AS A DYNAMIC THREE-DIMENSIONAL NETWORK COMPOSED OF STRUCTURAL AND SIGNALING MOLECULES, INCLUDING COLLAGENS, ELASTIN, FIBRONECTIN, PROTEOGLYCANS, AND GLYCOSAMINOGLYCANS, REGULATES ESSENTIAL CELLULAR PROCESSES SUCH AS PROLIFERATION, SURVIVAL, MIGRATION, AND DIFFERENTIATION. ALTERATIONS IN ECM COMPOSITION AND ORGANIZATION CONTRIBUTE SIGNIFICANTLY TO TUMOR GROWTH, INVASION, AND METASTASIS. AMONG ECM COMPONENTS, ELASTIN IS A HIGHLY STABLE PROTEIN RESPONSIBLE FOR MAINTAINING TISSUE ELASTICITY. DURING AGING AND PATHOLOGICAL CONDITIONS, ELASTIN UNDERGOES PROTEOLYTIC DEGRADATION, LEADING TO THE RELEASE OF BIOACTIVE ELASTIN-DERIVED PEPTIDES (EDPS).
THESE PEPTIDES HAVE BEEN SHOWN TO MODULATE MULTIPLE CELLULAR PROCESSES ASSOCIATED WITH CANCER PROGRESSION, INCLUDING MIGRATION, INVASION, AND METASTATIC DISSEMINATION. DESPITE EXTENSIVE RESEARCH USING CONVENTIONAL TWO-DIMENSIONAL (2D) CELL CULTURE SYSTEMS, SUCH MODELS FAIL TO FULLY REPRODUCE THE COMPLEXITY OF THE IN VIVO TUMOR ENVIRONMENT. IN CONTRAST, THREE-DIMENSIONAL (3D) SPHEROID CULTURES BETTER MIMIC CELL-CELL AND CELL-ECM INTERACTIONS, PROVIDING A MORE PHYSIOLOGICALLY RELEVANT PLATFORM FOR STUDYING TUMOR BEHAVIOR.
The present study investigated the effects of EDPs, using kappa-elastin (kE) as an experimental model, on breast cancer cells cultured under both 2D and 3D conditions. The highly invasive triple-negative breast cancer cell line MDA-MB-231 and its ERβ-suppressed counterpart were employed to evaluate the potential involvement of estrogen receptor β (ERβ) in mediating the cellular responses to kE. Functional assays were performed to assess spheroid formation, migration, dissemination, and invasive capacity following kE treatment. In parallel, molecular analyses were conducted to examine the expression of genes and proteins associated with extracellular matrix remodeling, epithelial-to-mesenchymal transition (EMT), and the elastin receptor complex (ERC). Overall, the results demonstrate that kE modulates breast cancer cell behavior in a manner dependent on both the cellular microenvironment and ERβ expression status. These findings provide further evidence for the role of elastin-derived peptides in breast cancer progression and highlight the importance of 3D culture models as more representative systems for investigating tumor biology and microenvironmental interactions.
Name: Marios Vetoulas
Title: Exploring Integrin-Matrix interactions in 2D and 3D ECM contexts in Breast Cancer Models
Supervisor: Nikos K. Karamanos, Professor
Date: 15/6/2026
Time: 10.00
Link: https://upatras-gr.zoom.us/j/92702932162?pwd=oo2u933CgpbJ8SdUGVXkhyXLuLRGfj.1
Abstract
Breast cancer progression is strongly shaped by interactions between tumor cells and the extracellular matrix (ECM). ECM composition, culture dimensionality and integrin-mediated matrix sensing regulate key processes such as adhesion, spheroid organization, dissemination and gene expression. In this study, Hs578T and shERβ MDA-MB-231 breast cancer cells were used to investigate how collagen type I, fibronectin, HA and sulfated HA (sHA, ~50 kDa) affect tumor cell behavior in 2D and 3D ECM contexts. Multicellular tumor spheroids were used to evaluatespheroid growth, matrix-dependent organization and dissemination under matrix-free, collagen type I-, fibronectin- and mixed collagen / fibronectin-containing conditions. In parallel, HA and sHA treatments were applied to assess their effects on spheroid behavior and ECM-dependent responses. Bioinformatic analyses supported the selection of collagen- and fibronectin-associated integrin subunits, which were further examined by real-time qPCR under 2D and 3D cell culture conditions.
The results showed that ECM composition strongly influenced spheroid organization and dissemination. Collagen type I promoted greater outward dissemination, whereas fibronectin-rich matrices were associated with more compact organization and reduced spreading. sHA altered spheroid growth dynamics and disrupted organized spheroid formation within ECM-rich environments, suggesting that it acts as a bioactive modulator of tumor cell–matrix interactions. Integrins’ expression analyses further revealed model-dependent remodeling, with shERβ MDA-MB-231 cells showing broader induction of adhesion-related integrins, while Hs578T cells displayed stronger dimensionality-driven downregulation of selected matrix-associated integrins together with consistent ITGB3 induction. Overall, these findings highlight the importance of integrin–ECM communication in breast cancer cell behavior and support further investigation of sulfated HA as an ECM-associated molecule with anti-cancer relevance in 3D breast cancer models.
Name: Panagiota Megremi
Title: Effect of simvastatin in the presence of hormones on syndecans expression of TNBC cells. An experimental and in silico study.
Date: 5 June 2026
Time: 11:00 am
Zoom link: https://upatras-gr.zoom.us/j/92702932162?pwd=oo2u933CgpbJ8SdUGVXkhyXLuLRGfj.1
Abstract
Triple-negative breast cancer (TNBC) is considered one of the most aggressive and heterogeneous subtypes of breast cancer due to the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). The limited availability of targeted therapies and the poor prognosis associated with TNBC highlight the need for the identification of novel molecular mechanisms and therapeutic approaches. Syndecans act as co-receptors and, together with extracellular matrix-related receptors, such as CD44 and RHAMM, participate in tumor progression, invasion, metastasis, and cell signaling. In parallel, increasing evidence suggests that statins, particularly lipophilic statins such as simvastatin, exhibit anti-cancer properties through inhibition of the mevalonate pathway and modulation of signaling pathways related to cell proliferation and survival.
In the present study, the effect of simvastatin on the functional properties of highly metastatic triple-negative breast cancer cells, MDA-MB-231 (ERα-/ERβ+) and Hs578T (ERα-/ERβ-), as well as on the expression of specific cellular components related to invasion, metastasis was investigated. The results were correlated with patient databases regarding the expression of these components and their impact on patient survival. Treatment with simvastatin demonstrated a similar cytostatic effect in both cell lines, Hs578T and MDA-MB-231, with IC50 value being 1.018 μΜ and 1.022 μΜ, respectively, suggesting that simvastatin progressively reduces cell viability.
Cell circularity in both cell lines was increased at higher simvastatin concentrations. The sequential increase in simvastatin concentration seemed to progressively alter the morphology, as the cells gradually changed from elongated to circular. At higher simvastatin concentrations, the cells were quite stressed and were found in aggregates, while some of them were dead.
The findings also suggest that simvastatin modulates the expression of extracellular matrix-associated genes in TNBC cells, while hormonal stimulation further influences these effects in a cell type-dependent manner. Alterations in syndecan and CD44 expression patterns indicate a potential involvement of these molecules in the cellular response to simvastatin and hormonal signaling. Moreover, bioinformatics analyses supported the clinical relevance of several studied genes in breast cancer prognosis and progression.
Overall, this study highlights the complex interplay between simvastatin, steroid hormones, and extracellular matrix-associated molecules in TNBC. The results contribute to a better understanding of the molecular mechanisms underlying TNBC progression and support the potential therapeutic value of simvastatin as an adjuvant strategy in aggressive breast cancer subtypes.
Three-member Evaluation Committee
Demitrios Vynios
Professor, Department of Chemistry, Supervisor
Nikos K. Karamanos
Professor, Department of Chemistry
Achilleas D. Theocharis
Professor, Department of Chemistry
Name: Maria-Georgia Drosinou
Title: Sulfated hyaluronan modulates extracellular matrix composition and miRNA expression in 3D breast cancer spheroids
Date: 5 June 2026
Time: 10:00 am
Zoom link: https://upatras-gr.zoom.us/j/92702932162?pwd=oo2u933CgpbJ8SdUGVXkhyXLuLRGfj.1
Abstract
Cancer remains one of the most common diseases worldwide, as incidence rates increase steadily. Breast cancer is a biologically heterogeneous disease due to the existence of several molecular subtypes and varying clinical behavior. Extracellular matrix (ECM) is a three-dimensional (3D) macromolecular network, that not only provides structural support to cells, but also plays a critical role in regulating cell functional properties under both physiological and pathological conditions. Hyaluronan (HA), the only non-sulfated glycosaminoglycan (GAG), regulates breast cancer progression in a size-dependent manner. Our group has previously demonstrated that chemically sulfated hyaluronan (sHA) reduces the aggressive phenotype and ECM-related gene expression in triple-negative breast cancer cells, while inhibiting tumor growth in vivo. Within the tumor microenvironment (TME), ECM becomes notably stiffer due to the high accumulation of matrix components, which promotes tumor growth. Furthermore, microRNAs (miRNAs) are recognized as key epigenetic regulators and constituents of the TME, influencing cellular functions, including proliferation, migration, invasion, metastasis, and resistance to chemotherapy. MiRNAs are endogenous, non-coding short RNA molecules that regulate gene expression through post-transcriptional mechanisms. Depending the functional roles of target-mRNA, they regulate the expression of crucial matrix effectors, while vice versa interactions within the TME influence miRNA expression. In this context, our research group has demonstrated the functional role of specific miRNAs in the regulation of matrix expression, signaling and breast cancer cell behavior. Despite the insights provided by traditional 2D cultures in cancer research, they inadequately model the structural and biochemical complexity of the TME. As a result, cancer research focuses on 3D culture models that better reproduce the dynamic cell–matrix interactions found in solid tumors. This MSc thesis aimed to evaluate the effects of 50 kDa fragments of non-sulfated HA and sHA on the expression of key matrix macromolecules, including matrix metalloproteinases, proteoglycans, and HA receptors, as well as specific miRNAs involved in breast cancer progression (e.g., miR-10b-5p, miR-200b-3p, let-7d-5p) enriched with bioinformatic analysis by Kaplan-Meier Plotter and RAIN association and interaction networks. In addition, we investigated the impact of sHA on spheroid growth and functional properties in 3D cultures of breast cancer cells with distinct estrogen receptor (ER) status. Our findings demonstrated that sHA exerts significant inhibitory effects on breast cancer progression in 3D models and distinct miRNA expression profiles depending on ER status. Collectively, these findings will contribute to new molecular insights on the role of sHA in matrix and miRNA regulation during breast cancer progression, potentially guiding the development of novel matrix-based therapeutic strategies targeting aggressive breast cancer subtypes.
Three-member Evaluation Comittee
Zoi Piperigkou
Assistant Professor, Department of Chemistry, Supervisor
Nikos K. Karamanos
Professor, Department of Chemistry
Demitrios Vynios
Professor, Department of Chemistry
Πληροφορίες στο επισυναπτόμενο.
Πληροφορίες στα επισυναπτόμενα.
Name: Astaras Stelios
Title: The anatomical site, the developmental stage and the differentiation state direct the vulnerability of human mesenchymal cells to UVB radiation.
Supervisor: Dr. Dimitris Kletsas, Research Director
Date: May 8, 2026
Ώρα: 11:00
Place: https://upatras-gr.zoom.us/j/92702932162?pwd=oo2u933CgpbJ8SdUGVXkhyXLuLRGfj.1
ABSTRACT
Skin is the largest organ in humans and because of its location it is characterized as the first defense against biological, environmental and physicochemical insults. Skin is categorized into three layers, the epidermis that is the outermost part of the organ, the dermis that is the main part of the organ and the hypodermis. Fibroblasts are the major cellular components of the dermis and the main extracellular matrix
(ECM) producers. Due to its outermost anatomical location skin is continuously exposed to solar ultraviolet (UV) radiation. The more energetic UVB wavelength (280–315 nm) is mainly absorbed by the epidermis; however, a ~5–10% of its photons reach and affect the upper part of the dermis. On the other hand, UVB radiation is considered as the main effector of premature skin ageing (the so-called photoaging), characterized among others, by skin fibroblasts’ death and premature senescence.
In a previous work of our laboratory it was shown that physiologically relevant UVB radiation doses are cytotoxic and provoke apoptosis to human skin fibroblasts, while the cells possess an arsenal of synergistically acting protective signaling pathways, with JNKs/ATM-p53 activation and interplay being indispensable for the cellular resistance towards UVB radiation and the maintenance of cell viability (Mavrogonatou et al., 2022). Aim of the present work was to explore if the different anatomical sites experiencing a different exposure to UVB radiation play a role in the vulnerability of UVB-treated fibroblasts and what are the molecular mechanisms underlying the resistance of fibroblasts to UVB-induced apoptosis.
Our results show that fibroblasts derived from the face are more resistant to UVB radiation compared to those derived from the arm or the lung. Interestingly, skin and lung fibroblasts from human fetuses are much more vulnerable to UVB radiation, compared to their counterparts from adult donors. Even more intriguingly, human adult adipose-derived mesenchymal stem cells have similar LD50 values with fetal fibroblasts.
Interestingly, JNKs/ATM-p53 axis does not seem to play a photoprotective role in all other cell types. Finally, in all cases an activation of the apoptotic machinery is occurring, as shown by the intense down-regulation of the anti-apoptotic gene BCL-2.
To conclude, these data indicate that the anatomical position, the developmental stage and the level of differentiation direct the vulnerability to UVB radiation, which adds to the well know heterogeneity of human mesenchymal cells. Moreover, the variance in the anti-oxidant capacity, the response to DNA damage and the activation of the apoptotic machinery are involved in the above-mentioned differences and the clarification of the underlying mechanisms may lead to novel photoprotective approaches.
Three-membered inquiry Committee
1. Dimitris Kletsas, Research Director (Supervisor)
Laboratory of Cell Proliferation and Ageing, Institute of Biosciences and Applications, NCSR “Demokritos”
2. Nikos Karamanos, Professor
Biochemistry, Biochemical Analysis & Matrix Pathobiology Research Group, Laboratory of Biochemistry, Department of Chemistry, University of Patras
3. Eleni Mavrogonatou, Senior Researcher
Laboratory of Cell Proliferation and Ageing, Institute of Biosciences and Applications, NCSR “Demokritos”
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ΑΙΤΗΣΗ ΥΠΟΨΗΦΙΟΤΗΤΑΣ ΔΠΜΣ ΕΦΑΡΜΟΣΜΕΝΗ BIOXHMEIA 2026-27