Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth: Roles of cyclic AMP and p38 mitogen-activated protein kinase

Figure 2 Growth inhibition of Hep3B cells by FACL4 knockdown (A) siRNA expression construction and predicated siRNA transcripts. (B) Colony formation assay. ^aP<0.05 vs mock or empty. pcDNA/FL, sense expression plasmid; pcDNA/antiFL, FACL4 antisense expression plasmid; pKd/non, non-specific siRNA expression plasmid; pKd/FL, FACL4 siRNA expression plasmid. (C-E) Cells transfected with pKd/non or pKd/FL2 plasmid and selected neomycin-resistant clones.

Figure 1 Up-regulation of FACL4 expression in HCC. P’t, patients; T, tumor from HCC; N, normal liver tissue from the same patient.

Figure 3 Effect of cAMP on the expression of FACL4 in Hep3B cells (A) and on the inhibition of p38 in Hep3B cells (B). In Figure 3B, a: total p38 proteins and the phorphorylated p38 by Western blot; b: the p38 kinase activity by in vitro kinase assay. ^aP<0.05 vs control.

Figure 4 Effect of p38 inhibitor on the expression of FACL4 in Hep3B cells. ^aP<0.05 vs control.

Figure 5 Up-regulation of phosphorylated p38 in human HCC. HCC tumor tissues (B, D, and E) and the non-cancerous tissues (A and C) were analyzed for the phosphorylated p38 (p-p38) by immunohistochemistry staining. Green arrows indicate the representative p-p38 immunoreactive cells (brown) (400×).