WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7150
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Article Encapsulation of IR783 in UiO-66 MOFs for Improved Photodynamic Efficacy Against Breast Cancer Cells(OICC Press, 2025) Sahinoglu, Sinem; Sanli-Mohamed, GulsahBreast cancer remains the most prevalent malignancy among women worldwide, underscoring the need for innovative therapeutic strategies beyond conventional modalities. Photodynamic therapy (PDT) offers a non-invasive approach that leverages light-activated photosensitizers to induce reactive oxygen species (ROS)-mediated tumor cell death. IR783, a near-infrared fluorescent (NIRF) heptamethine cyanine dye, has shown promise as a theranostic agent in cancer therapy due to its tumor-selective uptake and pro-apoptotic effects. However, its clinical potential is hindered by poor stability, rapid dissociation in polar environments, low quantum yield, and suboptimal tumor accumulation. In this study, we developed a multifunctional nanoplatform by encapsulating IR783 into UiO-66, a zirconium-based metal-organic framework (MOF), to enhance the delivery and photodynamic performance of the dye (IR783@UiO-66). The system was structurally characterized, and its biocompatibility and drug release profiles were evaluated. In vitro experiments were conducted to assess the cytotoxic and phototoxic effects of IR783, UiO-66, and IR783@UiO-66 on breast cancer cell lines (MCF-7, MDA-MB-231) and normal breast epithelial cells (MCF-10A), under LED irradiation at varying light intensities (18-144 J/cm2) and exposure durations (7.5-60 min). The results demonstrated that IR783@UiO-66 significantly reduced cancer cell viability in a dose-and light-dependent manner while sparing normal cells. Free IR783 showed slightly higher phototoxicity, attributed to differences in release kinetics and loading efficiency. UiO-66 alone exhibited negligible cytotoxicity under irradiation, confirming its safety profile. This study highlights the potential of UiO-66 as a promising nanocarrier for enhancing IR783-mediated PDT, offering a synergistic strategy for targeted and efficient breast cancer therapy.Article Cx32 Cellular Localization Is Related To Epithelial To Mesenchymal Transition in Breast Cells(Pleiades Publishing inc, 2025) Oz, Sercan; Turan, Fatma Basak; Yondem, Eyup; Pesen-Okvur, Devrim; Yalcin-Ozuysal, Ozden; Ozcivici, Engin; Mese, GulistanConnexins (Cx) play both gap junction-related and -independent roles in cells, and their localization is essential for their function in cellular processes. Besides membrane localization, connexins can also be localized to the cytoplasm and nucleus, especially in cancer cells. The differential localization of connexins including Cx32 was observed in different stages of cancers. Cx32 was upregulated and observed in cytoplasms of cells in lymph-node metastasis of breast cancer samples compared to primary tumors. However, the significance of the increase in Cx32 expression and alteration of Cx32 cellular localization in epithelial-to-mesenchymal transition (EMT) is not known. To determine if Cx32 overexpression and/or localization over one week would induce the EMT process, we first examined the cellular localization of Cx32 in MCF10A and MDA-MB-231 cells at different time points using Western blot and RT-PCR as well as immunostaining with confocal microscopy. Then, we correlated the changes of Cx32 expression and localization with EMT marker expression. We showed that Cx32 had altered cellular localization and Cx32 overexpression increased Slug levels while it reduced E-cadherin and Snail expression in MDA-MB-231 for 7 days. In contrast, E-cadherin and Vimentin were reduced in MCF10A-Cx32 cells compared with controls over 7 days, and the expression pattern for nuclear Cx32 and Zeb2 was following similar pattern in MCF10A cells. Our results suggest a previously unknown time-dependent relation between Cx32 and the regulation of the EMT process.Article Comprehensive Analysis Of<i> Gjb1</I> in Breast Cancer: Its Implications in Survival and Molecular Mechanisms(int inst Anticancer Research, 2024) Ozcivici, Engin; Mese, GulistanBackground/Aim: Breast cancer is the leading cause of cancer-related mortality among women worldwide. The connexin (Cx) family, including GJB1 (Cx32), plays complex roles in tumor progression depending on cellular context and cancer subtype. While Cx32 overexpression has been linked to lymph node metastasis, its effects on survival and molecular processes remain unclear. Herein, we aimed to investigate the role of GJB1 in breast cancer by examining its impact on survival and cellular processes in addition to its expression pattern in tumor subtypes, using public datasets. Materials and Methods: We conducted a comprehensive analysis of GJB1 in breast cancer using METABRIC patient dataset, Cancer Cell Line Encylopedia, and other publicly available databases. We examined the association between GJB1 expression and patient survival, performed differential gene expression analysis, and explored gene set enrichment to identify biological processes associated with high GJB1 expression. Results: GJB1 was significantly down-regulated in breast cancer tissues compared to normal tissues. However, patients with high GJB1 expression had significantly poorer survival compared to those with low expression, with the median survival reduced by over 25 months. Gene ontology (GO) analysis revealed that down- regulated genes in the GJB1-high group were enriched in extracellular matrix components and membrane junctions, while up-regulated genes were associated with mitochondrial function and cellular respiration. Conclusion: Our findings suggest a dual role for GJB1 in breast cancer. Although it is generally down-regulated, high GJB1 expression is associated with poorer survival, implying a potential oncogenic role. Further studies are needed to clarify the role of GJB1 in breast cancer and explore its therapeutic implications.