SELENOM-Knockdown Enhances the Protective Effect of A-172 Cancer Cells Against MSA-Induced ER–Stress and Staurosporine–Induced Apoptosis

SELENOM is a highly conserved protein, presented in different species and classes of animals, belongs to the family of thioredoxin–like folding proteins. It is known that SELENOM is more expressed in the brain and is very sensitive to selenium deficiency in this organ; it is involved in the regulation of calcium signaling, redox homeostasis, and apoptosis in brain cells. This study showed that SELENOM–knockdown in human glioblastoma cells (A–172 cell line) contributed to a decrease in the number of apoptotic A–172 cells after 24 or 48 h treatment with the known apoptosis inducer staurosporine, as well as a significant decrease in the number of necrotic cells after 48 h treatment with this inductor. A decrease in SELENOM ​​activity also led to a decrease in the Ca²⁺ ER–buffer capacity and influenced the level of mRNA expression of key ER–stress markers in glioblastoma cells.