Effect of recombinant adenovirus Ad5F35-SH2-DED on tumorigenicity of K562 cells in nude mice
10.3781/j.issn.1000-7431.2012.06.003
- Author:
Jing-Rong DENG
1
Author Information
1. Department of Clinical Hematology
- Publication Type:Journal Article
- Keywords:
K562 cells;
Leukemia, myeloid;
Models, animal;
Receptors, death domain
- From:
Tumor
2012;32(6):408-412
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effect of fusion protein SD (SH2-DED) on the K562 leukemia subcutaneous xenografts in nude mice. Methods: The models of K562 leukemia subcutaneous xenografts in nude mice based on pretreatment and treatment with recombinant adenovirus were established. In the pretreatment model, the K562 cells pretreated with recombinant adenoviruse Ad5F35-SD or its mutant Ad5F35-SmD were subcutaneously injected into the nude mice; in the treatment model, the K562 cells were firstly subcutaneously injected into the nude mice to induce the subcutaneous xenografts, and then the recombinant adenoviruse Ad5F35-SD or its mutant Ad5F35-SmD was intratumorally injected into the xenografts. The growth of the subcutaneous xenografts and the morphological changes of the tumor cells were observed. The apoptosis of the tumor cells in subcutaneous xenografts was detected by TUNEL method and observed under a transmission electron microscope. The expression levels of caspase-3 and caspase-8 proteins in the xenografts were examined by immunohistochemistry. Results: In the treatment model, the volume of subcutaneous xenografts was significantly inhibited by Ad5F35-SD treatment, and the pathological results showed nuclear condensation and deep staining of cytoplasm. The apoptosis of tumor cells was confirmed by TUNEL method and transmission electron microscopy. The expressions of apoptosis-associated proteins caspase-3 and caspase-8 were increased. In the pretreatment model, the growth of xenografts was also inhibited by pretreatment with Ad5F35-SD. Conclusion: Recombinant adenovirus Ad5F35-SD can inhibit the tumorigenicity of K562 cells and the growth of tumor xenografts in nude mice, and promote the apoptosis of tumor cells. © 2012 by Tumor.