Fig. 5

Nelfinavir inhibited cell viability and yields anti-tumor effects in LUAD cells. A Kaplan–Meier plotter showed the survival of LUAD patients in high expression group and low expression group of PPP2R1A. B mIHC showed the level of PPP2R1A in adjacent tissues and tumor tissues of LUAD patients (n = 5). C RT-qPCR was used to detect the mRNA level of PPP2R1A. D CCK8 assay measured the viability of BEAS-2B, A549 and PC9 cell lines under 0 (Control, DMSO), 5, 10, 20, 40 and 60 μmol nelfinavir treatment. E CCK8 assay measured the viability of BEAS-2B, A549 and PC9 cell lines under 0 (Control, DMSO), 25, 50, 100, 200, and 300 μmol velnacrine treatment. F,G CCK8 assay measured the viability of A549 (C) and PC9 (D) cell lines after 24 h of treatment with nelfinavir (10 μmol)/ cisplatin (10 μmol) or their combination. H Cell viability of PC9 cells treated with 20 μM Nelfinavir for 24 h in combination with ferroptosis inhibitor ferrostatin-1(Fer-1), apoptosis inhibitor Z-VAD-FMK, autophagy inhibitor 3-methyladenine(3-MA), necroptosis inhibitor necrostatin-1(Nec-1) and pyroptosis inhibitor 2-Bromohexadecanoic acid (2-BP). I Representative images of cell death after 24 h-treatment with nelfinavir (10 μmol)/ cisplatin (10 μmol) or their combination detected by flow cytometry. J Percentages of early-stage and late-stage apoptotic cells were compared among the four groups. K Western blot demonstrated that nelfinavir treatment induced the cleavage of caspase 3 and GSDME in PC9