TOXOPLASMA GONDII AS A FACTOR OF PROGRESSION OF CARCINOGENIC PROCESSES AT THE MOLECULAR-GENETIC LEVEL IN AN INTERMEDIATE HOST

Abstract

Objectives. To study Toxoplasma gondii as a factor of carcinogenic processes progression at the molecular-genetic level in an intermediate host. Material and methods. In the experiment, the expression of the proto-oncogenes survivin (BIRC5), epidermal growth factor (ErbB-2/HER2-Neu), GLI, vascular endothelial growth factor (VEGF) and anti-oncogene TP53 was determined in comparison with the reference genes - β-actin (ACTB) and GAPDH by means of PCR analysis in the tissues of animals with C6 tumor in situ infected with toxoplasma in different doses. A statistical comparison was made between the data of the experimental groups, depending on the dose of infection and the stage of the parasite development. Results. It has been revealed that toxoplasma can cause an increase in the expression of survivin (BIRC5), VEGF, ErbB-2/HER2-Neu, GLI in the tumors, lungs, liver, spleen, brain, both when invaded at a dose of 25 toxoplasma tachyzoites per 1 g of body weight (5000 tachyzoites per female) and when infected at a dose of 50 toxoplasma tachyzoites per 1 g of body weight (10000 tachyzoites per female). The degree of an increased expression of proto-oncogenes is directly dependent on the dose and stage of the parasite development. Infection of female rats having glioma with toxoplasma tachyzoites leads to a decrease in the expression of the anti-oncogene TP53 in the tissues of glioma, the lungs, liver, spleen, and brain of female rats. The decrease in the expression of TP53 depends on the dose of infection and the stage of toxoplasma development. Conclusions. Experimental toxoplasmosis causes an increase in the expression of BIRC5, ErbB-2/HER2-Neu, GLI, VEGF and a decrease in the expression of the anti-oncogene TP53, which can lead to the development of aggressive blastomogenic processes in mammalian tissues.