RESUMO
Breast cancer is one of the most prevalent malignancies and the leading cause of cancerassociated mortality in women worldwide and in China. Everolimus (C53H83NO14) is an efficient anti-cancer drug for breast cancer which targets mammalian target of rapamycin (mTOR). The present study investigated the inhibitory effects of everolimus on breast cancer cells and an MCF7bearing mouse model. The potential mechanism of the everolimusmediated decrease in growth and aggressiveness of breast cancer cells was reported. Results demonstrated that everolimus significantly inhibited breast cancer cell growth, migration and invasion. It was demonstrated that everolimus induced apoptosis through decreasing B cell lymphoma (Bcl)2 and Bclw and increasing caspase3 and caspase8 expression levels in breast cancer cells. It was observed that everolimus decreased phosphoinositide 3kinase (PI3K), protein kinase B (AKT) and mTOR expression levels in breast cancer cells. Results additionally demonstrated that PI3 K overexpression prevented that everolimusmediated inhibition of growth and aggressiveness in MCF7 cells. In vivo assays demonstrated that everolimus treatment markedly inhibited tumor growth in the MCF7 bearing mouse model. Overall, these data indicate that everolimus inhibits growth and aggressiveness of breast cancer cells through the PI3K/AKT/mTOR signaling pathways, suggesting the PI3K/AKT/mTOR signaling pathway may act as a therapeutic target for the treatment of human cancer.