Fig. 5: Pyroptosis of S34F mutant U2AF1-expressing cells as induced by FOXO3a-mediated NLRP3 inflammasome activation. | Cell Death & Disease

Fig. 5: Pyroptosis of S34F mutant U2AF1-expressing cells as induced by FOXO3a-mediated NLRP3 inflammasome activation.

From: U2AF1 mutation promotes tumorigenicity through facilitating autophagy flux mediated by FOXO3a activation in myelodysplastic syndromes

Fig. 5

A The proliferation curve of SKM-1 cells superinfected by FoxO3a-shRNA lentiviral particles at the specified time point. Then silencing of FOXO3a overcame the suppressive growth of S34F mutant U2AF1. B FOXO3a suppression abolished the induction of cellular apoptosis in S34F mutant U2AF1-expressing cells by flow cytometry using Annexin V single-staining. Overexpression of FOXO3a (FOXO3a-OE) rescued the growth capacity induced by S34F-shRNA-FoxO3a in SKM-1 cells. C, D Western blotting or qRT-PCR assays for NLRP3 inflammasome or other inflammatory biomarkers in SKM-1 or K562 cells treated with wild-type and S34F mutant U2AF1 for 96 h. E Western blotting analysis for FOXO3a and NLRP3 inflammasome markers in SKM-1 cells expressing wild-type U2AF1 and S34F mutant U2AF1 after transfection with the FOXO3a-shRNA lentiviral particles for 96 h. Band intensities represent values relative to control group. F, G Representative photomicrographs showed cells expressing S34F mutant U2AF1 containing green fluorescence protein (green) immunolabeled using the anti-FOXO3a and anti-NLRP3 antibody (red). Nuclei were stained with DAPI (blue). Scale bar, 50 µm. Magnification, ×200. Upper histogram represents quantification analysis. The data are presented as the means ± SD of multiple experiments conducted in triplicate. *p < 0.05, *p < 0.01, and ***p < 0.001. WT wild-type.

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