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To investigate the apoptosis\u2010inducing effect of MCFAs in breast cancer cells, cell viability assay, colony formation assay, cell migration assay, cell invasion assay, nuclear morphology, cell cycle assay, intracellular reactive oxygen species (ROS), matrix metalloproteinase (MMP), apoptosis, RT\u2010qPCR analysis, and Western blot analysis were performed. In the present study, MCFA treatments reduced proliferative capability, increased ROS level, increased the depletion of MMP, induced G0\/G1 and S phase cell cycle arrest, and late apoptosis of breast cancer cells in an effective concentration. Besides, MCFA treatment contributed to the upregulation of proapoptotic protein (BAK) and caspase\u20103, and the downregulation of antiapoptotic protein (Bcl\u20102). Mechanistically, phosphorylation levels of EGFR, Akt, and mTOR were significantly reduced in breast cancer cells treated with MCFAs. However, no significant changes in apoptosis and signaling\u2010related proteins were observed in lauric acid\u2010treated ER\u2010positive cancer cells. Our findings suggested that MCFAs suppressed breast cancer cell proliferation by modulating the PI3K\/Akt\/mTOR signaling pathway. MCFAs may be a promising therapeutic drug for treating breast cancer.<\/jats:p>","DOI":"10.1002\/jcb.30571","type":"journal-article","created":{"date-parts":[[2024,4,26]],"date-time":"2024-04-26T09:55:12Z","timestamp":1714125312000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Inhibitory effects of medium\u2010chain fatty acids on the proliferation of human breast cancer cells via suppression of Akt\/mTOR pathway and modulating the Bcl\u20102 family protein"],"prefix":"10.1002","volume":"125","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8674-9933","authenticated-orcid":false,"given":"P. 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