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Fig. 3 | Journal of Translational Medicine

Fig. 3

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

Fig. 3

CDK1 inhibitor CurE inhibited proliferation of ACC cells in vitro and in vivo. a IC50 values (CCK-8 assay) of CDK1 inhibitors indicated that CurE had the best dose-dependent inhibitory activity in SW-13 and NCI-H295R cells. b Chemical structure of CurE. c IC50 values of CurE on SW-13 cells at 24, 48 and 72 h were 0.19, 0.13 and 0.11 μmol/L, respectively. IC50 values of CurE on NCI-H295R cells at 24, 48 and 72 h were 1.632, 0.732 and 0.464 μmol/L respectively. d CurE dose-dependently suppressed the invasion and migration of SW-13 and NCI-H295R cells. e CurE dose-dependently suppressed soft agar colony formation of SW-13 and NCI-H295R cells. f Diagram of xenograft experiment in nude mice for assessing antitumor effects of CurE. g Images of xenograft tumors of each group. Animal experiments were grouped as follows: vehicle, Mtn (40 mg/kg), CurE (10 mg/kg), CurE (20 mg/kg) and co-administration of Mtn (40 mg/kg) and CurE (10 mg/kg). h–i CurE dose-dependently reduced tumor weight h and tumor volume i, and its inhibitory effect was greater than that of the positive drug, Mtn; tumors in the drug combination group almost disappeared. j Body weight remained stable during drug administration in each group. k Relative organ weights showed no significant differences between groups. Data was shown as mean ± SD. ##P < 0.01 vs. Mtn group, ***P < 0.001, **P < 0.01, *P < 0.05 vs. vehicle group

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