Μελέτη της συμβολής επιλεγμένων ρυθμιστών της οξειδοαναγωγικής κατάστασης στη διαφορική κυτταροτοξικότητα του CAP σε κύτταρα καρκίνου του μαστού

Cancer is characterized by the uncontrolled growth and proliferation of abnormal cells, with breast cancer representing one of the most prevalent malignancies worldwide. Breast cancer is a highly heterogeneous disease comprising distinct molecular subtypes, including Luminal A, Luminal B, HER2-positive, and triple-negative breast cancer (TNBC), which differ in their biological characteristics and responses to therapy. Despite significant advances in breast cancer treatment, the development of novel therapeutic approaches with improved efficacy and selectivity remains an important clinical need. Cold atmospheric plasma (CAP) has emerged as a promising anticancer technology whose biological effects are largely mediated by the generation of reactive oxygen and nitrogen species (RONS), leading to disruption of cellular redox homeostasis and oxidative stress. Previous findings from our laboratory, demonstrated differential sensitivity of breast cancer cell lines to direct dielectric barrier discharge CAP (DBD-CAP) treatment, suggesting that cell-specific mechanisms contribute to their distinct responses to plasma exposure. Based on these findings, the present study aimed to investigate whether differences in cellular redox regulation and antioxidant defense mechanisms contribute to the differential sensitivity of breast cancer cells to DBD-CAP. Particular emphasis was placed on the Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2)-mediated antioxidant responses and the glutaredoxin (Grx) system as important regulators of cellular redox homeostasis. In addition, hydrogen peroxide (H₂O₂) and lipid hydroperoxide (LOOH) levels were evaluated to characterize CAP-induced oxidative stress and lipid peroxidation, respectively, and to investigate their potential involvement in the differential sensitivity of breast cancer cells to DBD-CAP.