Objective To study the anti-breast cancer effects and molecular mechanisms of syringin, and to provide a theoretical basis for the clinical application of syringin.Methods The inhibitory effect of syringin on the proliferation of breast cancer cells was measured with MTT assay. Trypan blue, TdT-mediated dUTP nick-end labeling (TUNEL), and Annexin V-FITC/PI staining were used to detect apoptosis. Caspase-3 activation was detected via Western blot to determine whether apoptosis occurred. The expression of apoptosis-associated protein B-cell lymphoma-2 (Bcl-2) was detected and the effect of syringin on the mitochondrial apoptosis pathway was investigated via JC-1 staining. The PI3K agonist Recilisib was used for comparison. qRT-PCR and Western blot were used to assess the role of syringin in regulating the PI3K/Akt/mTOR pathway and inducing the apoptosis of cancer cells.Results Syringin had a time- and dose-dependent inhibitory effect on the proliferation of breast cancer cells and induced their apoptosis. A further study showed that after syringin treatment, Caspase-3 was activated, Bcl-2 expression decreased, the mitochondrial membrane potential was significantly reduced, and the mRNA and protein expressions of PI3K, Akt, and mTOR were not significantly changed, but the protein phosphorylation levels were significantly decreased. Recilisib partially limits the effect of syringin on the apoptosis of breast cancer cells.Conclusion Syringin has a good inhibitory effect on MDA-MB-231 and MCF-7 breast cancer cells. It can inhibit cell proliferation and induce mitochondrial apoptosis by inhibiting the activation of the PI3K/Akt/mTOR signaling pathway. Syringin is a potential anti-breast cancer drug.