Figure 4
ILK/β-catenin/p63 signaling cascade expressed by human OMECs isolated by dispase II/trypsin-EDTA (D/T) or collagenase (Col).
(A,B) Upon OMEC attachment to the basement membrane via integrin receptors, ILK is phosphorylated and activated. This not only phosphorylates and activates AKT but also phosphorylates and inactivates GSK-3β, such that β-catenin can avoid degradation and translocate to the nucleus. In the nucleus, β-catenin works with other transcription factors, such as TCF4, to turn on Wnt-associated genes, such as ΔNp63 and cyclin D1, to promote cell proliferation (activated ΔNp63 down-regulates p27KIP1). (C) Effect of ILK silencing on the signaling pathway. The causal relationship of the ILK/β-catenin/p63 pathway was confirmed by transfecting ILK siRNA into OMECs isolated by collagenase. Consequently, when the ILK pathway was blocked, nuclear β-catenin translocation, p63 expression, and cell cycle mediators were all significantly suppressed. (D) The immunoreactive band density of each experiment was quantified, first by normalization by the density of internal control (GAPDH or histone H3), then the relative signal intensity was expressed as D/T group divided by Col. group (with or without ILK silencing). Data are expressed as mean ± SD from three independent experiments. *p < 0.05. #Two test results with samples pooled from three donors.
