Association of platelet-derived growth factor receptor beta accumulation with increased oxidative stress and cellular injury in sestrin 2 silenced human glioblastoma cells.

摘要

Sestrin 2 (SESN2) is a stress-inducible protein required for maintaining redox homeostasis. However, its mode of action remains to be clarified. In this study, we found that SESN2 is induced in human glioblastoma U87 cells following ionizing radiation (IR). SESN2 silencing not only results in increased oxidative stress but also sensitizes U87 cells to IR. Intriguingly, we found SESN2 silencing significantly increases the expression of platelet-derived growth factor receptor beta (PDGFRbeta). Using a double knockdown technique, we showed that inhibition of PDGFRbeta accumulation in SESN2-silencing cells protects the cells from the deleterious effects induced by SESN2 silencing. Taken together, we revealed that PDGFRbeta accumulation is associated with increased oxidative stress and cellular damage in SESN2 silenced human glioblastoma U87 cells.