Cecropin-P17, an analog of Cecropin B, inhibits human hepatocellular carcinoma cell HepG-2 proliferation via regulation of ROS, Caspase, Bax, and Bcl-2

Cecropin‐P17 is a peptide derived from Cecropin B. In this study, we investigated the effects and relative mechanisms of Cecropin‐P17 in a human liver cancer cell line (HepG‐2) in vitro and in vivo. A cell viability assay, Annexin V/propidium iodide assay, western blot, flow cytometry, quantitative real‐time polymerase chain reaction, and a tumor‐xenograft model were applied to elucidate the mechanism exerted by Cecropin‐P17 on HepG‐2 cells. Cecropin‐P17 significantly inhibited the proliferation of HepG‐2 cells and demonstrated low cytotoxicity to normal liver cells in vitro. The apoptotic rate of HepG‐2 cells was increased after Cecropin‐P17 treatment together with increased production of reactive oxygen species. Moreover, Cecropin‐P17 stimulated caspase‐3, caspase‐9, and Bax and inhibited Bcl‐2 on both the transcriptional and translational levels. Finally, Cecropin‐P17 significantly suppressed tumor growth in a HepG‐2‐bearing nude mouse model. All of these results indicated that Cecropin‐P17 could be a potential agent for the treatment of liver cancer. Copyright © 2015 European Peptide Society and John Wiley & Sons, Ltd. Cecropin‐P17 is a peptide derived from Cecropin B. Cecropin‐P17 inhibited HepG‐2 cells' proliferation and demonstrated low cytotoxicity to normal liver cells in vitro. The results revealed that Cecropin‐P17 exhibited apoptotic effects on HepG‐2 cells, which were dependent on promoting the generation of ROS and activating caspase‐3, caspase‐9, and Bax and inhibiting Bcl‐2. These interferences then further inhibited the tumor growth of HepG‐2 cells in vivo. These results highlight the therapeutic potential of Cecropin‐P17 in liver cancer therapy.