Figure 7

rGal3C regulates phosphorylation of FAK/SRC, integrin clustering and expression of proteins. (A) Phosphorylation of Erk1/2 at Thr202/Tyr204 and Akt at Ser472 were increased. Phosphorylation of FAK at Tyr397/Tyr925 and SRC at Tyr416 were suppressed, meanwhile expression of β-Catenin were decreased. Parallel experiments were progressed and representative results of three independent replicates were shown. (B) Relative abundance of β-Catenin and phosphorylated of Erk1/2, Akt, FAK/SRC and β-Catenin after rGal3C stimulating. Protein expression abundance was normalized to Actin. Results are representative of three independent experiments. (C) The total fluorescence of both galectin-3 and rGal3C of HepG2 cells treated by rGal3C was displayed by red fluorescence of Alexa 594 dye, while integrin clustering by green fluorescence of Alexa 488 dye. Normal HepG2 cells were used as control. (D) Both rGal3C and Dasatinib stimulating suppresses the phosphorylation of FAK at Tyr397/925 and SRC at Tyr416. Parallel experiments were progressed and representative results of three independent replicates were shown. (E) Relative abundance of phosphorylated FAK/SRC after rGal3C or Dasatinib stimulating. Protein expression abundance was normalized to Actin. Results are representative of three independent experiments. (F) Blocking of integrin/FAK/SRC signaling pathway by Dasatinib leads to the decrease of S100A11, Galectin-1, NDRG1, CD166 and CLU. Parallel experiments were progressed and representative results of three independent replicates were shown. (G) Relative abundance of CLU, NDRG1, CD166, Galectin-1 and S100A11 after Dasatinib stimulating. Protein expression abundance was normalized to tubulin. Results are representative of three independent experiments. Error bars indicate the mean ± SD. Con, untreated HepG2 cells; *p < 0.01.