Several data has reported that capilliposide, extracted from a
traditional Chinese medicine, Lysimachia capillipes Hemsl. (LC) could exhibit inhibitory effect on cell proliferation in various
cancers. The current study investigated the antitumor efficacy of Capilliposide and elucidated its potential molecular mechanism involved in vivo and vitro. Our results indicated that
LC capilliposide inhibited proliferation of
lung cancer cells in a dose-dependent manner.
LC capilliposide induced cell cycle arrest at the S stage and enhanced apoptosis in NSCLC cells. Treatment with
LC capilliposide increased the intracellular level of ROS, which activated the mitochondrial apoptotic pathway. Blockage of ROS by NAC highly reversed the effect of
LC capilliposide on apoptosis. Xenograft
tumor growth was significantly lower in the LC-treated group compared with the untreated control group (P < 0.05). The results also show that LC treatment does not produce any overt signs of acute toxicity in vivo. These findings demonstrate that
LC capilliposide could exert an anti-
tumor effect on NSCLC through mitochondrial-mediated apoptotic pathway and the activation of ROS is involved.