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Fig. 1 | Journal of Translational Medicine

Fig. 1

From: Cycling hypoxia induces chemoresistance through the activation of reactive oxygen species-mediated B-cell lymphoma extra-long pathway in glioblastoma multiforme

Fig. 1

ROS is required for cycling hypoxia-mediated HIF-1α and NF-κB activation. The levels of nuclear HIF-1α and p65 (a), HIF-1 dependent transactivation of luciferase activity (b), NF-κB-dependent transactivation of luciferase activity (c), and intracellular ROS (d) in U251and U87 glioblastoma cells exposed to normoxia (Nor), uninterrupted hypoxia (NiH), or cycling hypoxia (CyH) (<1% O2) with or without Tempol. TATA-binding protein (TBP) was used to normalize protein loading for nuclear extracts. Error bars denote the standard deviation within triplicate experiments. **P < 0.01, ***P < 0.001 compared to normoxia. #P < 0.05, ###P < 0.001 compared to vehicle treatment

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