Inhibitory effects of 5-heptadecylresorcinol on the proliferation of human MCF-7 breast cancer cells through modulating PI3K/Akt/mTOR pathway

The effect of 5-heptadecylresorcinol (AR-C17) on the proliferation of human MCF-7 breast cancer cells was investigated in the present study. The results showed that AR-C17 treatment significantly suppressed MCF-7 cells proliferation, trigged intracellular ROS generation and decreased SOD2 expression. Furthermore, AR-C17 treatment could lead to MCF-7 cells apoptosis as evidenced by the activation of Bax/Bcl-2 expression ratio, active caspase activity and downregulation of mitochondrial membrane potential. Meanwhile, AR-C17 could activate MCF-7 cells autophagy by upregulating the protein levels of Atg7, Beclin-1 and LC3-II as well as decreasing SQSTM1/p62 and increasing autophagosomes formation in cytoplasm. Inhibition of autophagy with chloroquine (CQ) enhanced AR-C17-induced cell apoptosis. In addition, AR-C17 exerted anti-cancer activity through modulating PI3K/Akt/mTOR signaling pathway which was evidenced by decreasing the protein expression of PI3K, p-Akt and p-mTOR. Co-treatment with PI3K agonist IGF-1 could alleviate the inhibitory effect of AR-C17. Taken together, AR-C17 could be used as potential nutraceutical for breast cancer management.