Inhibition of the Expression of NRF2 Transcription Factor Mediated by miR-155 Causes a Decrease in the Viability of Melanoma Cells Regardless of Redox Status
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Abstract
The NFE2L2 gene of the redox-sensitive transcription factor NRF2 is a target of miR-155 microRNA. In the present work, a transfection of miR-155 imitator (mimic) was performed into dacarbazine-resistant B16 melanoma cells. It was determined that, under the influence of miR-155 microRNA mimic, the expression level of NRF2 encoded by the NFE2L2 decreases in melanoma cells both in conditions of oxidative stress and without it. A decrease in the level of NRF2 was accompanied by a decrease in the viability of dacarbazine-resistant melanoma cells. Thus, miR-155-mediated activation of NRF2, which regulates the intensity of antioxidant processes in the cell, can be associated with the preservation of viability and development of drug resistance of tumor cells. The latter can be used to overcome chemoresistance in the treatment of oncological diseases.
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The journal publishes papers on vast aspects of cell research, including morphology, biochemistry, biophysics, genetics, molecular biology, immunology. The journal accepts original experimental studies, theoretical articles suggesting novel principles and approaches, presentations of new hypotheses, reviews highlighting major developments in cell biology, discussions. The main objective of the journal is to provide a competent representation and integration of research made on cells (animal and plant cells, both in vivo and in cell culture) offering insight into the structure and functions of live cells as a whole. Characteristically, the journal publishes articles on biology of free-living and parasitic protists, which, unlike Metazoa, are eukaryotic organisms at the cellular level of organization.
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