Influence of tumor suppressor gene PTEN expression on biological behaviors of radiation-induced mouse thymoma cells
10.3724/SP.J.1008.2008.00888
- Author:
Bai-Long LI
1
Author Information
1. Department of Radiation Medicine
- Publication Type:Journal Article
- Keywords:
PTEN;
Rad51;
Radiation;
Thyoma
- From:
Academic Journal of Second Military Medical University
2010;29(8):888-891
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the expression of tumor suppressor gene PTEN in the radiation-induced mouse thymoma cells, and to observe the inhibitory effect of exogenous PTEN transfection on the in vitro proliferation and in vivo tumor forming ability of radiation-induced thymoma. Methods: Immunohistochemistry SP and Western blotting assay were used to examine the expression of PTEN, γ-H2AX, and Rad51 protein in radiation-induced mice thymoma and normal thymus tissues. RT-PCR assay was conducted to examine the PTEN gene loss. Exogenous PTEN gene was transferred into mouse thymoma cells and its inhibitory effects on cell proliferation and tumor-forming ability were observed. Results: The positive rate of PTEN protein expression was 22.73% (5/22) in radiation-induced thymoma tissue, significantly lower than that in the normal thymus tissue (P < 0.01). Western blotting assay showed that the expression of PTEN protein in thymoma was markedly lower than that in the normal thymus tissue (P<0.01). RT-PCR found that in tumor tissue there was high-frequency of PTEN gene loss. Exogenous PTEN expression in thymoma significantly inhibited the cell proliferation and the tumor-forming ability (P<0.01). The expression of γ-H2AX protein in the thymoma tissue was significantly higher than that in the normal thymus tissue; the expression of Rad51 protein was significantly lower than that in the normal tissue. Conclusion: Loss of PTEN gene may contribute to radiation-induced thymoma via influencing the Rad51-mediated DNA repair pathway. Exogenous PTEN gene transfer can inhibit the in vitro proliferation of thymoma cells, which may contribute to the treatment and prevention of radiation-induced tumor.
