Blueberry flavonoids inhibit matrix metalloproteinase activity in DU145 human prostate cancer cells

DOIResolve DOI: http://doi.org/10.1139/o05-063
AuthorSearch for: ; Search for: ; Search for: ; Search for: ; Search for:
TypeArticle
Subjectblueberry flavonoids; MMP activity; prostate cancer cells
AbstractRegulation of the matrix metalloproteinases (MMPs), the major mediators of extracellular matrix (ECM) degradation, is crucial to regulate ECM proteolysis, which is important in metastasis. This study examined the effects of 3 flavonoid-enriched fractions (a crude fraction, an anthocyanin-enriched fraction, and a proanthocyanidin-enriched fraction), which were prepared from lowbush blueberries (Vaccinium angustifolium), on MMP activity in DU145 human prostate cancer cells in vitro. Using gelatin gel electrophoresis, MMP activity was evaluated from cells after 24-hr exposure to blueberry fractions. All fractions elicited an ability to decrease the activity of MMP-2 and MMP-9. Of the fractions tested, the proanthocyanidin-enriched fraction was found to be the most effective at inhibiting MMP activity in these cells. No induction of either necrotic or apoptotic cell death was noted in these cells in response to treatment with the blueberry fractions. These findings indicate that flavonoids from blueberry possess the ability to effectively decrease MMP activity, which may decrease overall ECM degradation. This ability may be important in controlling tumor metastasis formation.
Copyright noticeCopyright 2005 NRC Canada
LanguageEnglish
AffiliationNRC Institute for Marine Biosciences; National Research Council Canada; Aquatic and Crop Resource Development
Peer reviewedYes
NRC number1711
NPARC number3538300
Export citationExport as RIS
Report a correctionReport a correction
Record identifiere30053d6-ebbb-4d39-95ed-dd698adae507
Record created2009-03-01
Record modified2016-05-09
Bookmark and share
  • Share this page with Facebook (Opens in a new window)
  • Share this page with Twitter (Opens in a new window)
  • Share this page with Google+ (Opens in a new window)
  • Share this page with Delicious (Opens in a new window)