Fig. 6: SDC4/DDX23 axis is crucial for driving HepG2 proliferation and migration.
From: Therapeutic potential of targeting membrane-spanning proteoglycan SDC4 in hepatocellular carcinoma
a, b siSDC4 blocked ERK/JNK/P38 MAPK, cell cycle, and MMP9 signaling pathways. CDK1, CyclinB1, P53, MMP2/9 and non-phosphorylations/phosphorylations of ERK/JNK/P38 were determined by western blot in SDC4 knockdown HepG2 cells. c, d siDDX23 prevented JNK/P38 MAPK, cell cycle, and MMP2/9 signaling pathways. CDK1, CyclinB1, MMP2/9 and non-phosphorylations/phosphorylations of ERK/JNK/P38 were detected by western blot in DDX23 knockdown HepG2 cells. e Correlation analysis between bufalin-regulated and siSDC4-altered proteins in HepG2 cells. f Correlation analysis between bufalin-regulated and siDDX23-altered proteins in HepG2 cells. Each data point represented the protein level (CDK1, CyclinB1, MMP2/9, and non-phosphorylations/phosphorylations of ERK/JNK/P38) changed by both bufalin and siSDC4 or siDDX23 treatment. Statistical significance was measured by Pearson’s correlation test. Data are expressed as mean ± SD for three individual experiments. **P < 0.01 vs. control group; ns, not significant by ANOVA with Student’s t-test.
