〔Abstract〕 Objective To investigate the ferroptosis induced by sesamin in triple-negative breast cancer(TNBC)4T1 cells and its underlying mechanism.Methods The binding energy of sesamin with glutathione peroxidase 4(GPX4),solute carrier family 7 member 11(SLC7A11),and P53 was analyzed by molecular docking.Mouse TNBC cell line 4T1 was used as a model.Different concentrations of sesamin were administered to 4T1 cells.The effect of sesamin on cell viability was assessed using the cell counting kit 8(CCK-8).Transwell assay was used to evaluate the effect of sesamin on cell migration and invasion.The contents of Fe2+,malondialdehyde(MDA),and reduced glutathione(GSH) in the cells were measured using kits.2',7'-dichlorofluorescein diacetate(DCFH-DA)probe was employed to detect the content of reactive oxygen species(ROS) in cells.Real-time quantitative reverse transcription polymerase chain reaction(RT-qPCR) and Western blot were performed to evaluate the expression of GPX4,SLC7A11,and P53 at mRNA and protein levels.Results The binding energies of sesamin with GPX4,SLC7A11 and P53 were-21.46,-21.67,and-27.03 kJ/mol,respectively.Compared with the control group,the viability of 4T1 cells in different concentrations of sesamin groups decreased gradually(P 2+,MDA,and ROS in 4T1 cells of 20,40,and 80 μmol/L sesamin groups increased,and the content of GSH decreased.Compared with the control group,the mRNA and protein expression of GPX4 and SLC7A11 in 4T1 cells in the sesamin treatment group decreased,and the mRNA and protein expression of P53 increased(all P