Figure 3.

PI3K/AKT and MAPK signaling pathways are involved in HMGB1-induced migration. CSCC SCC13 cells were treated with/without HMGB1 (100 ng/ml) or GR (100 µM) for 24 h. At the end of treatment, the activation [phosphorylation (P)] of AKT, p85 PI3K, p38 and p42/44 MAPK was analyzed by western blotting. The whole cell lysates were prepared, resolved by SDS-PAGE and subjected to western blot analysis. The total (T)-AKT, −p85 PI3K, −p38 and −p42/44 MAPK were used as a loading control. Results shown are representative of three independent experiments and were qualified by densitometry. (A) AKT and p85 PI3K; (B) p38 MAPK and p42/44 MAPK. CSCC, cutaneous squamous cell carcinoma; HMGB1, high-mobility group box 1; PI3K, phosphoinositide 3-kinase; MAPK, mitogen-activated protein kinase; GR, glycyrrhizin.