@article{Turovsky2026, 
author = {Egor A. Turovsky and Elena G. Varlamova},
title = {Cellular Knockdown of SELENOM Promotes Apoptosis Induction in Human Glioblastoma (A-172) Cells via Redox Imbalance},
year = {2026},
journal = {BIOCELL},
volume = {50},
number = {2},
pages = {10},
keywords = {Glioblastoma, selenoprotein M, apoptosis, hyperthermia, oxidative stress, mitochondrial potential, staurosporine},
url = {https://www.sciopen.com/article/10.32604/biocell.2025.073728},
doi = {10.32604/biocell.2025.073728},
abstract = {ObjectivesGlioblastoma multiforme (GBM) is highly resistant to apoptosis. This study investigates the role of Selenoprotein M (SELENOM), a redox-regulating protein, in the response of human glioblastoma A-172 cells to staurosporine (STS) and hyperthermia.MethodsA stable SELENOM-knockdown (SELENOM-KD) cell line was created. We measured reactive oxygen species (ROS), mitochondrial membrane potential (ΔΨm), cell death, and apoptotic gene expression.ResultsSELENOM-KD increased basal ROS levels and induced mitochondrial dysfunction. It sensitized cells to STS-induced apoptosis, enhancing the upregulation of pro-apoptotic genes. Conversely, under hyperthermia (42°C), SELENOM-KD cells exhibited significant thermoresistance, with 52% survival vs. 99% death in controls, associated with suppressed pro-apoptotic signaling.ConclusionsSELENOM is a critical redox and mitochondrial regulator in GBM. Its loss produces a context-dependent effect on cell fate: sensitizing to chemical apoptosis while conferring resistance to hyperthermia. SELENOM expression is a promising predictive biomarker for stratifying GBM patients for hyperthermia-based therapies.}
}