Objective To investigate the effects and mechanisms of Staphylococcus aureus (S. aureus) infection on the growth of breast cancer cells in vitro.

Methods 20 strains infected by S.aureu in sterile body fluid and human triple negative-breast cancer 231 cell lines (MDA-MB-231) were collected from Department of Breast Surgery of the Second Affiliated Hospital of Dalian Medical University from November 2016 to November 2022, respectively. The expression rates of virulence genes in S. aureus were detected by PCR amplification. The optimal multiplicity of infection (MOI) and the symbiotic ability were determined using co-culture experiments. The adhesion characteristics and internalization process of S. aureus were observed by adhesion experiments and electron microscopy. The effects of S. aureus infection on the migration and proliferation of MDA-MB-231 cells were examined by scratch assays, Transwell chamber assay, and CCK-8 assay, respectively. The expression changes of epithelial-mesenchymal transition (EMT)-related proteins in MDA-MB-231 cells after S. aureus infection were analyzed by Western blot and immunofluorescence assay.

Results The carrying rates of four virulence genes of 20 strains were clfA (95.00%), LuED (75.00%), fnbB (50.00%) and fnbA (95.00%), respectively. Co-culture and adhesion experiments demonstrated that S. aureus exhibited significant adhesion properties and could stably coexist with MDA-MB-231 cells. Transmission electron microscope observed that S. aureus was able to successfully invade and internalize in MDA-MB-231 cells. Scratch assay, Transwell chamber assay, and CCK-8 assay showed that S. aureus infection significantly inhibited the proliferation and migration of MDA-MB-231 cells. Western blot and immunofluorescence assay results indicated that the expression level of E-Cadherin was significantly up-regulated, while those of N-Cadherin, Vimentin, and total β-Catenin were significantly down-regulated (all P ＜ 0.05).

Conclusion S. aureus infection significantly suppresses the proliferation and migration of MDA-MB-231 cells and inhibits the metastasis of MDA-MB-231 cells by suppressing the EMT process.