Fig. 5
From: Targeting polo-like kinase 1, a regulator of p53, in the treatment of adrenocortical carcinoma
Inhibition of PLK-1 restores p53 functioning: Since PLK-1 is a negative regulator of p53, inhibition of PLK-1 should restore p53 transactivation and apoptotic functions. a Treatment of H295R and SW-13 cells with BI-2536 resulted in the restoration of wild type p53’s transactivation functions as seen by the increased transcription of its downstream gene, CDKN1A (p21) determined by qRT-PCR. b However, BI-2536 treatment of the SW-13 did not increase the transcription of CDKN1A, as it is mutant for p53 and the mutation is predicted to decrease p53 transactivation functions. c Furthermore, inhibition of PLK-1 restored wild type p53’s apoptotic response in H295R cells as determined by the Caspase 3/7 Glo assay. d The apoptotic response was slightly delayed in the SW-13 cells with mutant p53 with maximum response observed at 48 h. Doxorubicin was used as a positive control for apoptosis. All experiments were done at least 3 individual times, and data are represented as means with standard error