RAD51-IN-1 induces DNA damage and promotes ROS-mediated apoptosis in ovarian cancer cells

Aim. RAD51 protein is frequently overexpressed in ovarian cancer and plays a critical role in cancer cell development and survival. This study aims to elucidate, how RAD51-IN-1-induced DNA damage and apoptosis contribute to anti-cancer effects in ovarian cancer cell lines (MDAH-2774 and OVCAR-3). Methods. This research explores the impact of RAD51-IN-1 on cell viability, colony formation, ROS levels, DNA damage, and apoptosis were assessed in MDAH-2774 and OVCAR cell lines through the application of the CVDK-8 viability kit, colony formation assays, DCFDA staining, Comet assays, and AO/ER double staining methods. Results. Ovarian cancer cell lines were treated with varying doses of RAD51-IN-1, which resulted in a dose-dependent decline in both cell viability and colony formation, with the IC50 value for RAD51-IN-1 being determined. Furthermore, as shown by DCFDA staining, an increase in intracellular reactive oxygen species (ROS) and DNA damage as measured by the Comet assay was observed following RAD51-IN-1 treatment. RAD51-IN-1 was found to induce apoptosis by acridine orange/ ethidium bromide staining. Conclusions. This study demonstrates that RAD51-IN-1 effectively induces DNA damage and ROS-dependent apoptosis in ovarian cancer cell lines. Although RAD51-IN-1 requires further in vitro and in vivo evaluation as a treatment in ovarian cancer cells, these findings provide preliminary evidence of its potential efficacy.