Fig. 6: MK-2206 treatment downregulated matrix metalloproteinase (MMP) 2/9 and inhibited vasculogenic mimicry (VM) formation. | Cell Death & Disease

Fig. 6: MK-2206 treatment downregulated matrix metalloproteinase (MMP) 2/9 and inhibited vasculogenic mimicry (VM) formation.

From: Tenascin-c mediated vasculogenic mimicry formation via regulation of MMP2/MMP9 in glioma

Fig. 6

a VM formation was assessed in U251 and A172 cells after exposure to the Akt phosphorylation inhibitor MK-2206 at 0, 5, 10, and 20 μM for 24 h. The number of VM structures decreased in a dose-dependent manner. (magnification: ×100; scale bar = 100 μm). b Immunoblotting revealed that MMP2/9 expression and Akt phosphorylation at both Ser473 and Thr308 residues were significantly downregulated in a dose-dependent manner after MK-2206 treatment. c Zymography revealed that MMP2 and MMP9 activity was inhibited after MK-2206 treatment. d Immunoblotting revealed that MMP2/9 expression and Akt phosphorylation at both Ser473 and Thr308 residues were increased after TNC treatment for 24 h and decreased upon combinatorial treatment with TNC and 10 μM MK-2206. e, f The VM formation assay revealed that VM structures increased after TNC treatment for 24 h and decreased upon combinatorial treatment with TNC and 10 μM MK-2206. g A model describing the mechanism of how TNC involved the regulation of VM formation process. (*p < 0.05, **p < 0.01, ***p < 0.001).

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