Cellular Knockdown of SELENOM Promotes Apoptosis Induction in Human Glioblastoma (A-172) Cells via Redox Imbalance

Glioblastoma 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.

A 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.

SELENOM-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.

SELENOM 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.