tricetin and Glioblastoma

tricetin has been researched along with Glioblastoma* in 1 studies

Other Studies

1 other study(ies) available for tricetin and Glioblastoma

ArticleYear
Tricetin suppresses the migration/invasion of human glioblastoma multiforme cells by inhibiting matrix metalloproteinase-2 through modulation of the expression and transcriptional activity of specificity protein 1.
    Expert opinion on therapeutic targets, 2015, Volume: 19, Issue:10

    Glioblastoma multiforme (GBM) is a severely invasive tumor that can be fatal because it is difficult to treat. Tricetin, a natural flavonoid, was demonstrated to inhibit the growth of various cancers, but the effect of tricetin on cancer motility is largely unknown.. In the present study, we examined the anti-invasive properties of tricetin in huwman GBM cells.. Our results showed that tricetin inhibited the migration/invasion of two GBM cell lines. We found that tricetin inhibited MMP-2 expression in the GBM cells. Real-time polymerase chain reaction and promoter activity assays indicated that tricetin inhibited MMP-2 expression at the transcriptional level. Such inhibitory effects were associated with the suppression of specificity protein-1 (SP-1) DNA-binding activity. An examination of clinical samples revealed a positive correlation between SP-1 and MMP-2 in glioma specimens, and higher expression levels were correlated with a worse probability of survival. Moreover, blocking the extracellular signal-regulated kinase (ERK) pathway also inhibited MMP-2-mediated cell motility, and further enhanced the anti-invasive ability of tricetin in GBM cells.. SP-1 is an important target of tricetin for suppressing MMP-2-mediated cell motility in GBM cells, and a combination of tricetin and an ERK inhibitor may be a good strategy for preventing GBM invasion.

    Topics: Cell Line, Tumor; Cell Movement; Chromones; Female; Glioblastoma; Humans; Matrix Metalloproteinase 2; Matrix Metalloproteinase Inhibitors; Neoplasm Invasiveness; Real-Time Polymerase Chain Reaction; Sp1 Transcription Factor

2015