Open AccessBovine lactoferricin P13 triggers ROS-mediated caspase-dependent apoptosis in SMMC7721 cells
Author(s) -
Lixiang Meng,
GeLiang Xu,
Jiansheng Li,
Wenbin Liu,
Weidong Jia,
Jun Ma,
Decheng Wei
Publication year - 2016
Publication title -
oncology letters
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2016.5415
Subject(s) - apoptosis , cell culture , cancer research , reactive oxygen species , in vivo , in vitro , chemistry , endocrinology , cytosol , cell , medicine , microbiology and biotechnology , biology , biochemistry , enzyme , genetics
Bovine lactoferricin P13 (LfcinB-P13) is a peptide derived from LfcinB. In the present study, the effect of LfcinB-P13 on the human liver cancer cell line SMMC7721 was investigated in vitro and in vivo . The results of the present study indicate that LfcinB-P13 significantly decreased SMMC7721 cell viability in vitro (P=0.032 vs. untreated cells), while exhibiting low cytotoxicity in the wild-type liver cell line L02. In addition, the rate of apoptosis in SMMC7721 cells was significantly increased following treatment with 40 and 60 µg/ml LfcinB-P13 (P=0.0053 vs. the control group), which was associated with an increase in the level of reactive oxygen species (ROS) and the activation of caspase-3 and -9. Furthermore, ROS chelation led to the suppression of LfcinB-P13-mediated caspase-3 and -9 activation in SMMC7721 cells. LfcinB-P13 was demonstrated to markedly inhibit tumor growth in an SMMC7721-xenograft nude mouse model. The results of the present study indicate that LfcinB-P13 is a novel candidate therapeutic agent for the treatment of liver cancer.