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. 2013 Jan 29;11(2):316–331. doi: 10.3390/md11020316

Figure 3.

Figure 3

The responsibility of ERK activation for asperolide A-induced p53-p21 regulated cell cycle arrest. (A) NCI-H460 cells were treated with or without 35 μM asperolide A for indicated time, and then cells were harvested and lysed. cyclin B1, CDC2, p-CDC2 (Tyr15), cdc25C, p-cdc25C (Ser216), p-p53 (Ser15), p21 (Waf1/Cip1) were analyzed by Western blotting assay. GAPDH was used as an equal loading control; (B) Total and phosphorylated MAPK members (JNK, p38, ERK) after treatment with 35μM asperolide A for indicated time; (C) NCI-H460 cells were pre-treated with 20μM MEK inhibitor (PD98059), 10μM JNK inhibitor (SP600125), or 20μM P38 inhibitor (SB203580) for 2h, followed by treatment with or without 35 μM asperolide A for 48 h and the total or activation forms of MEK, JNK and p38 were evaluated by western blotting; (D) Cells were pre-incubated in absence or presence of MAPK inhibitors, then treated with 35 μM asperolide A, followed by immunoblotting assay performed with antibodies specific for CDC2, p-p53 and p21. Results are representative of three separate experiments. GPDH is shown as protein loading control.