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

  • Rockey Chao (Contributor)
  • Jyh-Ming Chow (Contributor)
  • Yi Hsien Hsieh (Contributor)
  • Chi Kuan Chen (Contributor)
  • Wei-Jiunn Lee (Contributor)
  • Feng Koo Hsieh (Contributor)
  • Nuo Yi Yu (Contributor)
  • Ming Chih Chou (Contributor)
  • Chao-Wen Cheng (Contributor)
  • Shun Fa Yang (Contributor)
  • Ming-Hsien Chien (Contributor)

Dataset

Description

Objective: 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.Research design and methods: In the present study, we examined the anti-invasive properties of tricetin in huwman GBM cells.Results: 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.Conclusions: 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.
Date made availableJan 1 2015
PublisherUnknown Publisher

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