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. 2015 Feb 4;33(4):1630–1638. doi: 10.3892/or.2015.3782

Figure 5.

Figure 5

Extracellular HMGB1 increases ERK1/2 phosphorylation in gastric cancer cells. (A) Twenty-four hour serum-starved BGC-823 cells were subjected to 100 ng/ml HMGB1 for the indicated time period, and western blot analysis was performed for the phosphorylated forms of p-ERK1/2 (Thr202/Tyr204), p38 (Thr180/Tyr182), p-JNK (Thr183/Tyr185), p-AKT (Thr308) and their corresponding non-phosphorylated proteins. (B) Starved BGC-823 cells were pretreated with the MAPK inhibitor U0126 or the media (control) for 1 h and then treated with 100 ng/ml of HMGB1 for 30 min and subsequently phosphorylated and total ERK1/2 were detected by western blot analysis. (C) Cell lysates from the starved BGC-823 cells were treated with HMGB1 (100 ng/ml) with or without glycyrrhizic acid (GA) for 30 min and analyzed by anti-phospho-ERK1/2 (p-ERK1/2) antibodies. Data are from one of the three separate experiments. HMGB1, high mobility group box-B1; MAPK, mitogen-activated protein kinase.