Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0545120140240060756
Journal of Microbiology and Biotechnology
2014 Volume.24 No. 6 p.756 ~ p.764
Potentiation of Apoptin-Induced Apoptosis by Cecropin B-Like Antibacterial Peptide ABPs1 in Human HeLa Cervical Cancer Cell Lines is Associated with Membrane Pore Formation and Caspase-3 Activation
Basse Mame Birame

Wang Jigui
Yu Fuxian
Sun Jiazeng
Li Zhili
Liu Weiquan
Abstract
Apoptin, a chicken anemia virus-encoded protein, induces apoptosis in chicken or human tumor cells, localizing in their nuclei as opposed to the cytoplasm of non-transformed cells. The present study was undertaken to investigate whether ABPs1 could potentiate apoptininduced apoptosis in HeLa cells. ABPs1 and the apoptin genes were successfully cloned into pIRES2-EGFP expression vector and expressed in HeLa cells. We report that ABPs1 augments apoptin cell growth inhibition in a concentration- and time-dependent manner. The DAPI staining and scanning electron microscopy observations revealed apoptotic bodies and plasma membrane pores, which were attributed to apoptin and ABPs1, respectively. Further, ABPs1 in combination with apoptin was found to increase the expression of Bax and to decrease the expression of survivin compared with either agent alone or the control. The apoptotic rate of HeLa cells treated with ABPs1 and apoptin in combination for 48 h was 53.95%. The two-gene combination increased the caspase-3 activity of HeLa cells. Taken together, our study suggests that ABPs1 combined with apoptin significantly inhibits HeLa cell proliferation, and induces cell apoptosis through membrane defects, up-regulation of Bax expression, down-regulation of survivin expression, and activation of the caspase-3 pathway. Thus, the combination of ABPs1 and apoptin could serve as a means to develop novel gene therapeutic agents against human cervical cancer.
KEYWORD
ABPs1, Apoptin, Apoptosis, Caspase-3, pores-forming, HeLa
FullTexts / Linksout information
Listed journal information
SCI(E) MEDLINE ÇмúÁøÈïÀç´Ü(KCI)