Figure 3

MIF targeting results in upregulation of contact inhibition markers and reduced mitogenic signaling. The antisense clones showed a restoration of contact inhibition indicated by increased expression of classical contact inhibition markers (p21, p27, p53 and C/EBPα) at lower cell densities (A). Densiometric quantification of the contact inhibitions markers relative to Actin of three independent experiments is shown in (B). Analysis of mitogenic signaling pathways revealed a marked reduction in basal Erk1/2 activity and a less pronounced reduction in Akt activity (C).