Objective To study the effect of nedaplatin on the proliferation, invasion, metastasis and apoptosis of breast cancer MDA-MB-231 cells, and explore the related mechanism. Methods Human breast cancer cell line MDA-MB-231 was cultured in vitro and divided into blank control group, positive control group (1 μmol/L docetaxel) and nedaplatin low, medium and high dose groups (15,30,45 μg/mL nedaplatin). The proliferation of MDA-MB-231 cells was detected by MTT assay. The apoptosis of MDA-MB-231 cells was detected by Annexin V-FITC/PI double staining. Transwell test and scratch test were used to detect cell invasion and migration; the changes of proliferating cell nuclear antigen (PCNA), B cell-lymphoma-2 (Bcl-2), Bcl-2associated X protein (Bax), invasion migration-associated proteins (E-cadherin), N-cadherin (N-cadherin) and Toll-like receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MyD88), nuclear transcription factor-kappa B (NF-κB), interleukin (IL-1β) and tumor necrosis factor-α (TNF-α) were detected by Western blot. Results Compared with that in the blank control group, the proliferation inhibition rate of MDA-MB-231 cells in low, medium and high dose nedaplatin groups was significantly increased at 24 and 48 h (P＜0.05), in a dose-dependent manner, and there was no significant difference between the high-dose group and the positive control group (P＞0.05). Compared with those in the blank control group, the apoptosis rate of MDA-MB-231 cells and Bcl-2, E-cadherin protein expression in low, medium and high dose nedaplatin groups were significantly increased (P＜0.05), the invasive cell number, cell migration rate and the expression levels of PCNA, Bax, N-cadherin, TLR4, MyD88, NF-κB, IL-1β and TNF-α were significantly decreased (P＜0.05), in a dose-dependent manner, there was no significant difference between high dose group and positive control group (P＞0.05). Conclusion Nedaplatin can inhibit the proliferation, invasion and migration of MDA-MB-231 cells and promote cell apoptosis, which may be realized by inhibitingthe activation of TLR4/NF-b signaling pathway.