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Inhibition of topoisomerase IIα: novel function of wedelolactone
Petr Benes, Lucia Knopfova, Filip Trcka, Alice Nemajerova, Diana Pinheiro, Karel Soucek, Miroslav Fojta, Jan Smarda
Jazyk angličtina Země Irsko
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NS9600
MZ0
CEP - Centrální evidence projektů
- MeSH
- antigeny nádorové metabolismus MeSH
- apoptóza účinky léků MeSH
- buněčný cyklus účinky léků MeSH
- buňky - růstové procesy účinky léků MeSH
- DNA vazebné proteiny antagonisté a inhibitory metabolismus MeSH
- DNA-topoisomerasy typu II metabolismus MeSH
- ELISA MeSH
- imunoblotting MeSH
- inhibitory topoisomeras farmakologie MeSH
- kumariny farmakologie MeSH
- lidé MeSH
- nádorové buněčné linie MeSH
- nádory prsu farmakoterapie enzymologie patologie MeSH
- poškození DNA MeSH
- protinádorové látky farmakologie MeSH
- signální transdukce MeSH
- viabilita buněk účinky léků MeSH
- Check Tag
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
The naturally occurring coumestan wedelolactone has been previously shown to reduce growth of various cancer cells. So far, the growth-suppressing effect of wedelolactone has been attributed to the inhibition of the NFκB transcription factor and/or androgen receptors. We found that wedelolactone suppressed growth and induced apoptosis of androgen receptor-negative MDA-MB-231 breast cancer cells at concentrations that did not inhibit the NFκB activity. The cells responded to wedelolactone by the S and G2/M phase cell cycle arrest and induction of the DNA damage signaling. Wedelolactone interacted with dsDNA and inhibited the activity of DNA topoisomerase IIα. We conclude that wedelolactone can act as growth suppressor independently of NFκB and androgen receptors.
Citace poskytuje Crossref.org
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- $a The naturally occurring coumestan wedelolactone has been previously shown to reduce growth of various cancer cells. So far, the growth-suppressing effect of wedelolactone has been attributed to the inhibition of the NFκB transcription factor and/or androgen receptors. We found that wedelolactone suppressed growth and induced apoptosis of androgen receptor-negative MDA-MB-231 breast cancer cells at concentrations that did not inhibit the NFκB activity. The cells responded to wedelolactone by the S and G2/M phase cell cycle arrest and induction of the DNA damage signaling. Wedelolactone interacted with dsDNA and inhibited the activity of DNA topoisomerase IIα. We conclude that wedelolactone can act as growth suppressor independently of NFκB and androgen receptors.
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