Fig. 6: The enhancing effect of SLC39A10 on the protein stability of CK2β and the holoenzyme activity of CK2.

a The effect of SLC39A10 knockdown on the holoenzyme activity of CK2 was evaluated by western blotting analysis (first two panels). In addition, SLC39A10-overexpressing AGS and MKN45 cells and control cells were treated with 3.5 μM TPEN, 5 μM silmitasertib (CX-4945, a selective CK2 inhibitor) or vehicle for 24 h, and the holoenzyme activity of CK2 was then quantified by western blotting analysis (the last four panels). β-Actin was used as a loading control. b SLC39A10-overexpressing AGS and MKN45 cells were treated with 5 μM CX-4945 for 24 h, and western blotting analysis was then performed to test the effect of CX-4945 treatment on MAPK/ERK and PI3K/AKT pathway activity. β-Actin was used as a loading control. c An MTT assay was carried out to evaluate cell proliferation in SLC39A10-overexpressing AGS and MKN45 cells and control cells with the indicated treatments. d The effect of SLC39A10 knockdown or overexpression on the protein expression of CK2α and CK2β was evaluated by western blotting analysis. β-Actin was used as a loading control. e SLC39A10-knockdown AGS and MKN45 cells and control cells were treated with 10 µM CHX for the indicated times, and CK2β protein expression was then evaluated by western blotting analysis (left panels). The band intensity of CK2β was normalized to that of β-Actin, and this value was then normalized to the corresponding value in the control cells (right panel). f The indicated cells were treated with 25 μM MG132 (a proteasome inhibitor) for 3 h, and the protein expression of SLC39A10 and CK2β was evaluated by western blotting analysis. β-Actin was used as a loading control. Data are presented as the means ± SDs. ***P < 0.001.