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Cecropin‐P17, an analog of Cecropin B, inhibits human hepatocellular carcinoma cell HepG‐2 proliferation via regulation of ROS, Caspase, Bax, and Bcl‐2
Author(s) -
Wu Chunli,
Geng Xiaoping,
Wan Shengyun,
Hou Hui,
Yu Fanzong,
Jia Benli,
Wang Lei
Publication year - 2015
Publication title -
journal of peptide science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.475
H-Index - 66
eISSN - 1099-1387
pISSN - 1075-2617
DOI - 10.1002/psc.2786
Subject(s) - propidium iodide , apoptosis , cecropin , microbiology and biotechnology , flow cytometry , in vitro , viability assay , cell culture , western blot , in vivo , annexin , chemistry , biology , peptide , biochemistry , programmed cell death , antimicrobial peptides , gene , genetics
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.