Research Paper Volume 12, Issue 22 pp 23114—23128
Intracellular and extracellular S100A9 trigger epithelial-mesenchymal transition and promote the invasive phenotype of pituitary adenoma through activation of AKT1
Figure 2. Extracellular S100A9 participated in proliferation, migration and invasion of PA through activation of AKT1. (A) The HP75 cells were divided into control group, recombinant S100A9 protein group and recombinant S100A9 protein+ A-674563 group. CCK-8 showed that the recombinant S100A9 protein accelerated proliferation at 24, 48, 72 and 96h. However, the recombinant S100A9 protein-mediated promotion of proliferation was partially reversed by the addition of an AKT1 inhibitor(A-674563). (B) Flow cytometry indicated that the recombinant S100A9 protein decreased the G0/G1 phase proportion and increased the S phase ratio, but these effects could be counteracted by A-674563. (C, D) The cell migration was analyzed by a wound-healing assay and a transwell insert system after treatment with the recombinant S100A9 protein alone or combined with A-674563. (E) The transwell assay also demonstrated that the recombinant S100A9 protein improved invasion of HP75 cells, but the function could be neutralized by A-674563. (n=5. *P<0.05; **P<0.01; ***P<0.001 vs. Control group. #P<0.05; ##P<0.01; ###P<0.001 vs. Recombinant S100A9 protein+ A-674563 group).