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. 2018 Jan 5;9(11):9885–9906. doi: 10.18632/oncotarget.24009

Figure 7. CP-B2RAs promote increased levels of the cell-cycle inhibitor p27kip and reduce clonogenic growth through p-38-dependent pathways.

Figure 7

Effects of NG68 and FR173657 on (A) the phosphorylation (and activity) status of MAPK p38, and (B) the expression of p27kip1. To detect the phosphorylation of p38, cells were treated with or without CP-B2RAs for the indicated times. To determine p27 expression, cells were treated with the same antagonists at indicated concentrations for 24h. Whole cell lysates were analyzed by western blotting using the indicated antibodies. β-actin was used as an internal loading control in each case. Representative autoradiograms of 2–3 experiments. Also added in panel B are the effects of the MAPK p38 inhibitor SB203580 (SB) on FR173657 and NG68-triggered expressions of p27kip1. Cells pretreated for 6h with SB (10 µM) were treated with CP-B2RAs at indicated concentrations for 24h. Whole cell lysates were prepared and analyzed by Western blot as in A. (C) Effects of MAPK p38 inhibitor, SB203580 on FR173657- and NG68-induced anti-clonogenic activities against MDA-MB-231 cells. Cells pretreated for 6h with SB (10 µM) were treated with or without CP-B2RAs at indicated concentrations for 14 days. Clonogenecity efficiency was evaluated as described in Figure 3; SB alone had no effect (not shown). Data are as mean ± s.e.m. of 6–8 experiments. Ctl, control (no treatment). *p < 0.05 versus the indicated group, using Student’s t-test for unpaired samples.