Figure 4

Activation of ERK1/2, p38and JNK induced by CXCL5 and role of ERK1/2 signal pathway in the chemotaxis of CXCL5 on LCCs. (A) Phosphorylated and total amounts of ERK1/2, p38 MAPK or JNK measured by Western blot in HepG2 and MHCC97H; (B) Ratio of p-ERK1/2/total ERK1/2, p-p38/total p38, p-JNK/total JNK in HepG2 and MHCC97H. (C) Effect of ERK1/2 inhibitor U0126 on CXCL5-induced migration and invasion of HepG2 measured by transwell assay (×200); (D) Average cell numbers of migration and invasion in three identical experiments (n = 3 each). (E) Effect of U0126 on CXCL5-induced migration and invasion of HepG2 measured by wound-healing assay (×100); (F) Levels of healing percent. GFP-HepG2 cells were pretreated with or without U0126 at 10 μM or DMSO for 2hs, followed by challenge with or without CXCL5 (controls) at 10 nM. (**P < 0.01, +P < 0.05, ++P < 0.01, +++P < 0.001).