CCK-8, Transwell migration Assay and Wound-healing assay were appraisal assays for cell proliferation and migration. qRT-PCR and western blot were performed to test the expression of miR-4262, MMP2, MMP13 and LATS1 in glioma cancers tissues and cancer cells.
Our research emphasized the suppressive function of miR-93-5p in glioma by targeting MMP2, thus providing some novel experimental basis for the treatment of glioma.
The FITC-iCREKA was proved to have significantly higher cellular uptake in the glioma U87 cells in the presence of activated MMP-2 than that in absence of activated MMP-2 by cells fluorescence test <i>in vitro</i>.
CD34-PAS staining was carried out to observe VM formation, and immunohistochemistry was used to determine the expression levels of Beclin-1, HIF-1α, VEGF and MMP2 in 105 patients with primary glioma.
Taken together, these results suggest that Migfilin is a critical regulator in cellular motility by driving the EGFR-MMP-2 feedback loop, and may be considered as a potential therapeutic target in glioma.
In conclusion, our data demonstrate that Diaph1 is highly expressed in human glioma, plays a significant role in glioma cell migration, and can influence the expression and activity of MMP2 and MMP9 indirectly in human glioma cell lines U87 and U251.
Similarly, relatively little is known about the relationship of miR-140-5p, vascular endothelial growth factor A, and matrix metalloproteinase-2 in glioma progression.
Furthermore, MALAT1-mediated tumor suppression in glioma cells may be via reduction of extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) signaling activity and expression of matrix metalloproteinase 2 (MMP2).
Transfection of miR-150-5p or miR-133a mimics into glioma cell lines reduced MT1-MMP expression and MMP-2 activation by these cells, and cell proliferation and invasion/migration were also suppressed by it.
In conclusion, our data suggest that SERPINB1 negatively regulates glioma cell migration and invasion probably by abrogating the expression of MMP-2 and the activation of FAK.
Matrix metalloproteinase 2, critical in human glioma migration and invasion, was down-regulated upon Girdin reduction and led to decreased invasion in vitro and in vivo.
Knockdown of MMP-2 using MMP-2 small interfering RNA (pM) in human glioma xenograft cell lines 4910 and 5310 decreased cell proliferation compared with mock and pSV (scrambled vector) treatments, as determined by 5-bromo-2'-deoxyuridine incorporation, Ki-67 staining and clonogenic survival assay.
Our studies on increased anoikis sensitization in matrix metalloproteinase-2 (MMP-2)-knockdown 4910 and 5310 human glioma xenograft cells were interestingly correlated with p21-activated kinase 4 (PAK4) inhibition, prompting us to further investigate the role of PAK4 in glioma.
By RT-PCR, glioma cell invasion assay showed that the expression of MMP-2 was increased in ppGalNAc-T2-knockdown cells, while the expression of MMP-9 and TGF-β1 was decreased in ppGalNAc-T2-overexpressing cells at the mRNA level.