Abstract—Sodium selenite, which is one of the most common selenium compounds, is considered a potential anticancer agent that can decrease cell viability; this compound is present in many types of malignant cells. Oxidative stress contributes to malignant transformation, in particular, by inducing prolonged endoplasmic reticulum stress due to a dramatic increase in free-radical levels. Selenoproteins are oxidoreductases that exhibit antioxidant activity due to the presence of selenium; thus, the need occurs to investigate the role of selenoproteins in the regulation of carcinogenic processes, with a focus on selenoproteins associated with the endoplasmic reticulum, which is an organelle with a high level of redox activity. Almost one-third of the currently known human selenoproteins are located in the endoplasmic reticulum; some of these have been shown to participate in the regulation of processes associated with stress of the endoplasmic reticulum in different types of tumor cells. In this work, changes in the expression patterns of endoplasmic reticulum-resident selenoprotein genes, as well as of key genes involved in the regulation of endoplasmic reticulum stress, were studied in human fibrosarcoma cells exposed to sodium selenite.
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ACKNOWLEDGMENTS
This work was supported by the Russian Foundation for Basic Research (projects nos. 17-04-00356 and 18-34-00118 mol_a) and a grant from the President of the Russian Federation for young scientists and post-graduate students (SP-2059.2016.4).
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Abbreviations: ER, endoplasmic reticulum; UPR, unfolded protein response; ROS, reactive oxygen species; CHOP, C/EBP-homologous protein; D2, iodothyronine deiodinase 2; SELK, SELN, SELS, SELM, SELT, SELI, and SEP15, selenoproteins K, N, S, M, T, I, and 15, respectively; GADD34, growth arrest and DNA damage protein 34; PCR, polymerase chain reaction.
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Varlamova, E.G., Goltyaev, M.V. The Effect of Sodium Selenite on the Expression of Genes of Endoplasmic Reticulum-Resident Selenoproteins in Human Fibrosarcoma Cells. BIOPHYSICS 63, 700–705 (2018). https://doi.org/10.1134/S000635091805024X
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DOI: https://doi.org/10.1134/S000635091805024X