Roles of GSK-3 in EGF-promoted glioma cell invasion.

<p>(A) EGF promoted U87 cell invasion in the transwell assay. ** <i>P</i><0.01 versus DMSO .(B) GSK-3 knock-down and uniform up-regulation of GSK-3β activities inhibited U87 cell invasion. * <i>P</i><0.05, ** <i>P</i><0.01 versus pcDNA3 (<i>ctl</i>) or non-sense control (<i>si-ctl</i>). (C) Up-regulation of p-Ser-GSK-3 levels during EGF-induced wound recovery of U251 cells. <i>Left</i>: representative western blots of U251 cell lysates collected at indicated time points after scratching. <i>Right</i>: statistics of pSer-GSK-3 levels normalized to GSK-3 levels and then compared with the value at 0hr. *<i>P</i><0.05, ** <i>P</i><0.01 versus the value of pGSK-3/GSK-3 at 0hr. (D) Location of increased pGSK-3 staining in EGF-induced wound recovery of U251 cells 3 hrs after scratching. <i>Green</i>: anti-pSer21-GSK-3αor anti-pSer9-GSK-3β; <i>Red</i>: rhodamine phalloidin. <i>Original magnification, 400×</i>. si-3α, siRNA against GSK-3α; si-3β, siRNA against GSK-3β; WT, wild-type form of GSK-3β; S9A, constitutively active form of GSK-3β. Data were mean ± SD of three independent experiments. EGF, 40ng/ml.