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Fig. 4 | Journal of Translational Medicine

Fig. 4

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

Fig. 4

CDK1 regulated G2/M phase transition of ACC cells through interaction with UBE2C and AURKA/B. a Overexpression of CDK1 promoted DNA synthesis of SW-13 cells, while CDK1 knockdown suppressed DNA synthesis in NCI-H295R cells. b Overexpression of CDK1 reduced the percentage of G2/M phase cells and increased S phase in SW-13 cells. c Knockdown of CDK1 expression blocked the G2/M transition of NCI-H295R cells. d CDK1 altered the expression of UBE2C and AURKA/B. e CDK1 interacted with UBE2C and AURKA/B. f CurE suppressed DNA synthesis of SW-13 cells. g CurE suppressed DNA synthesis of NCI-H295R cells. h CurE time- and dose-dependently suppressed the G2/M phase in SW-13 cells. i CurE time- and dose-dependently suppressed the G2/M phase of NCI-H295R cells. j CurE blocked phosphorylation of CDK1 and reduced UBE2C and AURKA/B expression. Experiments were performed in triplicate, and data was presented as mean ± SD. **P < 0.01, ***P < 0.001 vs. control group

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