Abstract: Background　Triple-negative breast cancer (TNBC), recognized as the most aggressive subtype with the poorest prognosis in breast cancer, has emerged as a critical research focus due to the lack of effective therapeutic targets. Ferroptosis, a novel form of programmed cell death, opens new avenues for tumor treatment. Objective　To construct a multifunctional nanotheranostic platform, Ce6@Fe3O4@PAD, and evaluate its therapeutic efficacy against triple-negative breast cancer 4T1 cells. Methods　The photosensitizer Ce6 and Fe3O4 nanoparticles were loaded onto PAD particles via self-assembly, and the materials were characterized using transmission electron microscopy and Malvern particle size analysis. Confocal laser scanning microscopy and flow cytometry were employed for qualitative and quantitative assessment of cellular uptake in 4T1 cells. Live/dead staining was performed to visualize cytotoxicity, while the IC ₅ ₀ value was quantitatively determined using the CCK-8 assay. Intracellular reactive oxygen species (ROS) accumulation was measured using fluorescence probes. Glutathione (GSH) and malondialdehyde (MDA) levels were quantified to assess redox status. Furthermore, Western blotting was utilized to detect changes in the key ferroptosis marker GPX4 to indicate the involvement of ferroptosis. Results　The Ce6@Fe3O4@PAD nanocomposite was successfully constructed, exhibiting an average hydrodynamic diameter of 135.5 nm and a zeta potential of -16.2 mV, which are suitable dimensions for drug delivery. The nanoparticles maintained stable particle sizes after incubation in solutions containing various concentrations of FBS and BSA for 24 h, demonstrating excellent potential for in vivo circulation. The loading efficiency of Ce6 in the nanocomposite was (6.0 ± 0.2)%. Confocal imaging and flow cytometry confirmed efficient cellular uptake by 4T1 cells. Live/dead staining revealed significant cytotoxic effects, and CCK-8 assays further verified low dark toxicity but potent phototoxic killing efficacy (P＜0.001), with an IC₅₀ of 8.68 μg/mL. Western blot analysis showed significant downregulation of GPX4 protein expression in the treatment group (P＜0.001). Concurrently, GSH levels decreased significantly while MDA levels increased substantially (P＜0.001), confirming that the platform induces ferroptosis by suppressing the antioxidant system.Conclusion　The Ce6@Fe3O4@PAD nanotheranostic platform induces ferroptosis through photodynamic therapy, demonstrating significant killing effects on triple-negative breast cancer cells. It provides a novel strategy to overcome clinical challenges in the diagnosis and treatment of triple-negative breast cancer.