Evaluation of the radiomodifying effects of Ginkgo biloba in radioresistant triple negative breast cancer cells

Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by limited therapeutic options and intrinsic resistance to ionizing radiation. Ginkgo biloba (GB) possesses documented anticancer, antioxidant and pro-apoptotic properties; however, its potential role as a radiomodifying agent remains insufficiently investigated. The present study evaluated the effects of GB on the radiation response of the radioresistant MDA-MB-231 TNBC cell line. Cells were treated with increasing concentrations of GB (10–350 μg/mL) either alone or in combination with a clinically relevant single dose of 3 Gy delivered using 6 MV X-ray photons (3 Gy/min). Cell viability was evaluated by the MTT assay, while intracellular reactive oxygen species (ROS) generation and apoptosis were assessed by flow cytometry using CellROX and Annexin V/propidium iodide (PI) staining, respectively. Statistical evaluation was performed using two-way analysis of variance (ANOVA) to assess the effects of GB pretreatment, irradiation and their interaction. GB pretreatment produced a significant concentration-dependent reduction in cell viability, demonstrating intrinsic cytotoxic activity at higher concentrations. In contrast, neither 3 Gy irradiation alone nor the interaction between GB pretreatment and irradiation significantly affected cell viability. Similarly, no significant effects of GB, irradiation or their interaction were detected for intracellular ROS generation or the percentage of live cells determined by flow cytometry. These findings indicate that, under the present experimental conditions, GB did not significantly modify the response of MDA-MB-231 cells to clinically relevant irradiation. In conclusion, GB exhibits concentration-dependent cytotoxic activity toward MDA-MB-231 cells but no statistically significant radiomodifying effects of GB were detectable following a single 3 Gy exposure using the investigated short-term cellular endpoints.