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. 2022 Jan 21;13(1):73. doi: 10.1038/s41419-022-04524-2

Fig. 2. NKAP knockdown induced cell death through ferroptosis.

Fig. 2

A Lipid peroxidation level in U87MG and U251 cells was influenced by NKAP knockdown assessed by C11-BODIPY using flow cytometry immunolabelling in the absence or presence of 0.5 μM ferrostatin-1 or 5 μM alpha-tocopherol for 24 h. B Lipid peroxidation level influenced by NKAP overexpression. C MDA level influenced by NKAP knockdown in the absence or presence of 0.5 μM ferrostatin-1 or 5 μM alpha-tocopherol for 24 h. D MDA level influenced by NKAP overexpression. E Transmission electron microscopy revealed the characteristics of NKAP knockdown U87MG cells. The white arrow indicated normal mitochondria. Black arrow indicated deeply stained, shrunken mitochondria. F The longest diameter of the mitochondria in the scramble (n = 6) and shNKAP (n = 6) group. G Effect of NKAP on the U87MG cell sensitivity to erastin (10 μM), iFSP1 (100 μM), SAS (500 μM), rotenone (2.5 μM), 17-DMAG (300 nM), staurosporine (1.5 μM), TMZ (200 μM), β-lapachone (2 μM), H2O2 (1‰), LPS (200 μg/ml), and rapamycin (300 nM). All drug treatments were for 24 h. H Cell viability of U87MG and U251 glioma cells when grown in 1, 2, 5, 10, 20, 50, and 100 μM erastin for 24 h. I Cell viability when grown in 0.01, 0.1, 1, 10, and 100 μM iFSP1 for 24 h. J Cell viability when grown in 0, 100, 250, 500, and 1000 μM SAS for 24 h. All bars show mean ± SD of three independent experiments. *P < 0.05, **P < 0.01.