Fig. 5: CDK16 inhibition promotes PRC1 delocalization to the nucleus and PRC1 accumulation.

a Analysis of PRC1 distribution in 293T AS-CDK16 cells after 3MBPP1 treatment (0, 5 and 10 µM) and subcellular fractionation. The columns represent the means ± SEMs of 9 independent experiments. b Representative images of PRC1 immunofluorescence (red) and the Na+/K+ATPase (membrane marker) in 293T AS-CDK16 cells treated with 0 (control), 5 or 10 µM 3MBPP1. c PRC1 accumulation in 293T and 293T AS-CDK16 cells treated with 3MBPP1 (0, 5 and 10 µM) for 6 h was assessed by western blotting. The columns represent the means ± SEMs of 12 independent experiments. *P < 0.05, **P < 0.01 vs control; Mann–Whitney test. d Analysis of PRC1 distribution in HT-29 colon cancer cells after treatment with dabrafenib (0, 2 and 10 nM) for 24 h and subcellular fractionation. The columns represent the means ± SEMs of 8 independent experiments. e Representative images of PRC1 immunofluorescence (red) and the Na+/K+ ATPase in HT-29 cells treated with 0 (control), 2 or 10 nM dabrafenib for 24 h. f PRC1 accumulation in HT-29 cells treated with 2 nM dabrafenib for 24 h was assessed by western blotting. The columns represent the means ± SEMs of 8 independent experiments. *P < 0.05 vs nontreated (NT) cells, Mann–Whitney test