THE EFFECT OF TOXOPLASMAS ON THE CHANGES IN THE EXPRESSION OF BIRC5, ERBB-2/HER2-NEU, GLI, VEGF PROTOONCOGENES AND THE ANTI-ONCOGENE TP53 IN RATS IN THE EXPERIMENT

Abstract

Objectives. To study the effect of toxoplasmas on the changes in the expression of protooncogenes BIRC5, ERBB-2/HER2-NEU, GLI, VEGF and the anti-oncogene TP53 in rats in an experiment depending on the infection dose and the period of parasite development. Material and methods.The experiment was conducted on female Wistar rats to determine changes in the expression of the protooncogenes survivin (BIRC5), epidermal growth factor (ErbB-2/HER2-Neu), GLI 1, vascular endothelial growth factor (VEGF) and the anti-oncogene TP53 in comparison with the reference genes β-actin (ACTB) and GAPDH by means of PCR analysis in the tissues of 10 healthy and 120 animals invaded at different doses. Statistical comparison of the results of all groups was drawn with the data of the «control» series (healthy animals, biopsies of the lungs, liver, spleen, brain). The results obtained in the experimental groups were as follows: the infection dose of 25 toxoplasma tachyzoites per 1 g of the animal body weight (5000 tachyzoites per female) and the infection dose of 50 toxoplasma tachyzoites per 1 g of the animal body weight (10000 tachyzoites per female), then they were also compared with each other. Statistical processing of the obtained data was carried out using the program Statistica 10.0. The differences were considered to be reliable at a significance level of less than 0.05 (p<0.05). Results. Toxoplasma was found to cause an infection dose-dependent increase in the expression of the protooncogenes survivin (BIRC5), epidermal growth factor (ErbB-2/HER2-Neu), GLI, vascular endothelial growth factor (VEGF) and a change in the strength expression of the anti-oncogene TP53 at all stages of the parasite development. Conclusions. Experimental toxoplasmosis alters the expression of the protooncogenes survivin (BIRC5), epidermal growth factor (ErbB-2/HER2-Neu), GLI, vascular endothelial growth factor (VEGF), and the anti-oncogene TP53 in the tissues of the intermediate host.