Fig. 2.

Cycling hypoxia mediates Bcl-xL expression via HIF-1α or NF-κB activation. Bcl-xL mRNA (a) and protein (b) levels in GBM8401 glioblastoma cells collected before and after 1 h of each of the 3 cycles of hypoxia (<1 % O₂) during cycling hypoxia (CyH) and after 4 h of uninterrupted hypoxia (NiH). *P < 0.05, **P < 0.01, ***P < 0.001 compared to normoxia. c Western blot analysis of HIF-1α or p65 knockdown in GBM8401 glioblastoma cells via the lentiviral-based HIF-1α or p65 shRNA. d, e Bcl-xL mRNA and protein levels in GBM8401 glioblastoma cells transfected with or without scramble (Scr.), HIF-1α, or p65 shRNA for 48 h followed by stimulation with cycling hypoxic stress for 4 h. ***P < 0.001 compared to normoxia (c). ^#P < 0.01, ^##P < 0.001 compared to Scr. shRNA treatment. f, g Bcl-xL mRNA and protein levels in U251 and U87 cells treated with cycling hypoxic stress for 4 h in the absence or presence of HIF-1α (YC-1) and NF-κB (Bay 11-7082) inhibitors. Error bars denote the standard deviation within triplicate experiments. ***P < 0.001 compared to normoxia (Nor). ^##P < 0.01, ^###P < 0.001 compared to vehicle treatment