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Fig. 5 | Journal of Translational Medicine

Fig. 5

From: CDK1 serves as a therapeutic target of adrenocortical carcinoma via regulating epithelial–mesenchymal transition, G2/M phase transition, and PANoptosis

Fig. 5

CDK1 inhibitor CurE induced apoptosis, pyroptosis, and necroptosis (PANoptosis) in ACC cells. a Effect of CurE on morphology of NCI-H295R and SW-13 cells at 3, 6 and 12 h. Spherical membranal protrusions were observed in NCI-H295R and SW-13 cells. b CurE caused the release of LDH from SW-13 and NCI-H295R cells. c The cytotoxicity of CurE could be partially rescued by combined treatment with Z-VAD-FMK (VAD) and necrosulfonamide (Nec), while it could not be restored by using them alone or using autophagy inhibitor 3-MA. d, e Annexin V-PI double staining showed that CurE increased the percentage of necrotic and apoptotic/pyroptotic SW-13 cells d and NCI-H295R e cells. f, i CurE time-dependently increased the expression of apoptosis marker protein, cleaved caspase 3/7, and altered the expression of other apoptosis-related proteins in SW-13 (f) and NCI-H295R (i) cells. g, j CurE time-dependently increased the expression of pyroptosis marker protein, GSDMD, and altered the expression of other pyroptosis-related proteins in SW-13 (g) and NCI-H295R (j) cells. h, k CurE time-dependently increased the expression of necroptosis marker protein, MLKL, and altered the expression of other necroptosis-related proteins in SW-13 (h) and NCI-H295R (k) cells. Experiments were performed in triplicate, and data was presented as mean ± SD. ***P < 0.001 vs. control group

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