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STRESS-DEPENDENT MOLECULAR MECHANISMS OF REGULATION OF GENE EXPRESSION DURING TUMOR GROWTH AND METABOLIC DISEASES
Ratushna O. O.
Кандидат біологічних наук
O. V. Palladin Institute of Biochemistry
Науковий співробітник
Цимбал Дарія Олександрівна
O. V. Palladin Institute of Biochemistry
Молодший науковий співробітник
Cycle of scientific works consists of 35 publications: 14 articles in scientific journals, 4 GenBank entries, 17 proceedings from conferences and meetings, which were published in a period from 2008 till 2015. Investigation of stress-dependent molecular mechanisms of regulation of gene expressions in different pathological conditions, such as tumor growth and metabolic diseases, is nowadays an important issue, because oncologic and metabolic diseases constantly spread. Aim of the study – investigation of molecular mechanisms of decreased proliferation of glioma cells and growth of gliomas upon inhibition of IRE1 (inositol requiring enzyme 1), a key signaling pathway of endoplasmic reticulum stress, as well as molecular mechanisms of obesity and its complications, by studying expression of genes, that control main metabolic cycles, proliferation and apoptosis. Main results – both in malignant tumors and in obesity and its complications (such as type II diabetes) a marked deregulation of glycolysis is observed. A key player in this process is fructose-2,6-bisphosphate. Synthesis and cleavage of fructose-2,6-bisphosphate is controlled by bifunctional enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB), which has many variants with different kinetic and regulatory characteristics. Moreover, expression of almost all PFKFB genes is decreased in obesity and insulin resistance and increased in tumors and under hypoxic conditions. During endoplasmic reticulum stress a genome reprogramming takes place, which functions to restore cellular homeostasis and prevent cell death. We found, that the following genes HOXC6 (homeobox C6), ATF3 (activating transcription factor 3), TBX3 (T-box 3), FOXF1 (forkhead box F1), EPAS1 (endothelial PAS domain protein 1), E2F8 (E2F transcription factor 8), MEST (mesoderm specific transcript), CD24 (CD24 antigen), KRT18 (cytokeratin 18), ING1 (inhibitor of growth 1), IL13RA2 (interleukin 13 receptor A2) take part in such reprogramming. The importance of conducted studies lays in deeper understanding of fundamental mechanisms of malignant growth inhibition and development of metabolic diseases. Obtained results can facilitate identification of new gene targets for development of new therapeutics.
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, 2023