
TRICHINOSIS AS A FACTOR DETERMINING THE CHANGE IN THE EXPRESSION OF PROTOONCOGENES AND SUPPRESSOR GENE IN EXPERIMENT
Author(s) -
V.V. Pabiarzhyn
Publication year - 2021
Publication title -
žurnal grodnenskogo gosudarstvennogo medicinskogo universiteta
Language(s) - English
Resource type - Journals
eISSN - 2413-0109
pISSN - 2221-8785
DOI - 10.25298/2221-8785-2021-19-1-91-95
Subject(s) - biology , glioma , survivin , trichinosis , pathology , gene expression , gene , immunology , cancer research , medicine , biochemistry , helminths
The aim is to study trichinosis as a factor determining changes in the expression of proto-oncogenes and the suppressor gene in an experiment. Material and methods. The experimental animals were divided into 3 groups. In female rats of the first («control with tumor») and second groups («glioma combined with trichinosis», infection at a dose of 20 Trichinella spiralis larvae per 1 gram of animal body weight) a C6 glioma tumor in situ was simulated. The sampling of material from animals of the first group was carried out on the 14th, 21st, 28th, 35th days of tumor development, respectively (tumor, liver, lungs, brain). In females of the second group, biopsies (tumor, liver, lungs, brain) were taken on the 7th (14th day of tumor development), 14th (21st day of tumor development), 21st (28th day of tumor development) tumor), on the 28th day after infection (35th day of tumor development) and in the third group, once (liver, lungs, brain). RNA was directly isolated from the material by the column method. Amplification was performed on a Real-Time PCR thermal cycler. Comparative expression of the studied genes was carried out after normalization of each of the samples to the level of the control genes GAPDH and ACTIN-β. Expression analysis was performed with qbase + and CFX Maestro software. Results. Host invasion with trichinella leads to an increase in the expression of survivin (BIRC5), GLI, VEGF and TP53 in the tissues of the lungs, liver and brain. Conclusion. Exposure to trichinella can trigger the initiation of carcinogenic processes and aggravate their course.