Anti-tumor effects on human laryngeal carcinoma Hep-2 of recombinant fowlpox virus expressing chicken anemia virus Apoptin gene.
- Author:
Guofang GUAN
1
;
Ningyi JIN
;
Xiao LI
;
Lili SUN
;
Chunshun JIN
;
Wei LOU
;
Ping SHI
;
Yanru HAO
Author Information
1. Department of Otorhinolaryngology, the Second Hospital, Bethune Faculty of Medical Sciences of Jilin University, Changchun, 130041, China. guan-guo@163.com
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
drug effects;
Capsid Proteins;
genetics;
pharmacology;
Chicken anemia virus;
genetics;
Fowlpox virus;
genetics;
Humans;
Tumor Cells, Cultured
- From:
Journal of Clinical Otorhinolaryngology Head and Neck Surgery
2009;23(6):264-270
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the anti-tumor effects and the mechanism of the recombinant fowlpox virus expressing Apoptin gene on human laryngeal carcinoma Hep-2.
METHOD:Hep-2 cells cultured in vitro were infected with vFVApoptin. The anti-tumor effects on Hep-2 cells were measured through MTT staining and, the mitochondrial trans-membrane potential (delta psi m) and reactive oxygen species (ROS) were analyzed by flow cytometry. Western blot was used to detect the release of cytochrome c (Cyto c). Caspase-3/9 activities were measured by colorimetric assay.
RESULT:vFVApoptin could restrain Hep-2 cells significantly and, had the function of down-regulating delta psi m, up-regulating ROS, promoting Cyto c release and activating Caspase-3/9.
CONCLUSION:Cyto c were released from mitochondria by the function of up-regulating ROS of vFVApoptin. Cyto c triggered Caspase-9 and, after the activation of Caspase-9, downstream apoptotic factors, such as caspase-3, were activated. Eventually, Hep-2 cells were suppressed by mitochondrial pathway apoptosis induced by vFVApoptin.
