The present study showed that as autophagy was inhibited, MDA-MB-231 cells exposed to BJE displayed higher phosphorylation of mTOR, PI3K, and Akt in vitro, and the MDA-MB-231 tumor tissue from BJE groups exhibited obviously higher phosphorylation of mTOR, implying that BJE is able to suppress autophagy via activating the PI3K/Akt/mTOR signaling pathway, thus blocking the development of TNBC. Here, AKT1 is linked to neoplasm.