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Activation of Signal Pathways of Apoptosis under Conditions of Prolonged ER-Stress Caused by Exposure of Mouse Testicular Teratoma Cells to Selenium-Containing Compounds.
Doklady Biochemistry and Biophysics ( IF 0.8 ) Pub Date : 2020-04-27 , DOI: 10.1134/s160767292001007x M V Goltyaev 1 , E G Varlamova 1 , S V Novoselov 1 , E E Fesenko 1
中文翻译:
小鼠睾丸畸胎瘤细胞暴露于含硒化合物导致的ER-应激延长时,凋亡信号通路的激活。
更新日期:2020-04-27
Doklady Biochemistry and Biophysics ( IF 0.8 ) Pub Date : 2020-04-27 , DOI: 10.1134/s160767292001007x M V Goltyaev 1 , E G Varlamova 1 , S V Novoselov 1 , E E Fesenko 1
Affiliation
Abstract
Aim to study the molecular mechanisms of apoptotic death of mouse testicular teratocarcinoma cells (line F-9) under exposure to the widely used selenium-containing compounds with antitumor activity, sodium selenite and methylseleninic acid. Methods fluorescence microscopy, MTT assay, Western blotting. Results It was shown that sodium selenite at a concentration of 10 μM and methylseleninic acid at concentrations of 1 and 10 μM cause apoptosis-dependent death of F-9 cells, excluding necrotic death. Western blotting showed an increase in the expression of XBP1s when treating F-9 cells with 1 μM methylseleninic acid. Conclusions 10 μM methylseleninic acid leads to cell apoptosis, most likely by activation of the IRE1 signaling pathway under prolonged stress of the endoplasmic reticulum.中文翻译:
小鼠睾丸畸胎瘤细胞暴露于含硒化合物导致的ER-应激延长时,凋亡信号通路的激活。