Fig. 2: p50 inhibited arsenite-induced autophagy, and in turn resulting in upregulation of HIF-1α protein accumulation following arsenite treatment.
From: NF-κB1 p50 stabilizes HIF-1α protein through suppression of ATG7-dependent autophagy
A, B WT, p50−/−, Beas-2B(Nonsense), and Beas-2B(shp50) cells were treated with 20 μM arsenite for 24 h. The cells were extracted and cell lysates were subjected to western blot assay by using the indicated antibodies. The ratio of LC3 II/LC3 I was quantified. C The GFP-LC3 construct was stably transfected into WT, and p50−/− cells, and the transfectants were treated with 20 μM arsenite for 24 h. LC3 puncta formation was observed and images were captured using fluorescence microscopy. D Percentage of cells with GFP-LC3 puncta (in above C) and number of puncta per positive cell were calculated and presented. The symbol (*) indicates a significant increase in comparison to WT cells treated with arsenite (p < 0.05). E WT, and p50−/− cells were treated with 20 μM arsenite, with or without 5 nM BAF for 24 h. the cell extracts were subjected to western blot for the determination of indicated protein expression. The ratio of LC3 II/LC3 I was quantified. β-Actin was used as protein loading control.
