Impact of the gene expression level and intermolecular interaction networks on radioresistance of tumor cells

Автор: Pogodina E.S., Rastorgueva E.V., Yurova E.V., Beloborodov E.A., Sugak D.E., Saenko Yu.V., Fomin A.N., Volkov M.A., Kostishko B.M.

Журнал: Ульяновский медико-биологический журнал @medbio-ulsu

Рубрика: Физиология

Статья в выпуске: 3, 2022 года.

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Despite its efficacy, radiation therapy faces the challenges connected with accelerated reproduction of tumor cells and radioresistance of malignant neoplasms. The aim of the study was to analyze the impact of the gene expression level and intermolecular interaction networks on the development of tumor cell radioresistance. Materials and Methods. The authors used 4 tumor cell lines: (K562, HCT-116p53 (+/+), HCT-116p53 (-/-), and Me45. To study the cell line transcriptome. Affymetrix high-density hybridization DNA chips (HGU133A series) were used. Bioinformatic analysis of gene expression dynamics was performed using the original Gene Selector program. Intermolecular interaction networks were studied using the STRING online system. Results. After exposure to ionizing radiation at a dose of 4 Gy, the expression level of DAAM1, IFNAR2, PALLD, and STK17A genes increases in K562 cell line and decreases in HCT-116p53 (+/+), HCT-116p53 (-/-) and Me45. Numerous protein complexes of the studied genes were found with STRING online system. Thus, DAAM1, IFNAR2, PALLD, and STK17A genes influence the activity of some particles in the network of intermolecular interactions. Selected DAAM1, IFNAR2, PALLD and STK17A genes and protein-protein complexes encoded by DAAM1, TNK2, PTBP2 and DVL2; IFNAR2, STAT2, IRF9, JAK1, GNB2L1 and IFNAR1; PALLD, LPP and ACTN2 genes can be used as potential targets. Their modulation can increase the response of malignant neoplasm cells to ionizing radiation.

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Malignant tumor, gene expression, tumor cell radioresistance, ionizing radiation, protein-protein interaction

Короткий адрес: https://sciup.org/14125352

IDR: 14125352   |   DOI: 10.34014/2227-1848-2022-3-142-155

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