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Switching p53-dependent growth arrest to apoptosis via the inhibition of DNA damage-activated kinases
Pavla Hublarova, Kristina Greplova, Jitka Holcakova, Borivoj Vojtesek,Roman Hrstka
Jazyk angličtina Země Polsko
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NS9812
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Zdroj
BioMedCentral Open Access od 2006
PubMed Central od 2006
Europe PubMed Central od 2006
ProQuest Central od 2006-03-01 do 2014-12-31
Health & Medicine (ProQuest) od 2006-03-01 do 2014-12-31
ROAD: Directory of Open Access Scholarly Resources od 2006
Springer Journals Complete - Open Access od 2006-03-01
Springer Nature OA/Free Journals od 2006-03-01
Odkazy
PubMed
20526748
DOI
10.2478/s11658-010-0021-5
Knihovny.cz E-zdroje
- MeSH
- antitumorózní látky farmakologie MeSH
- apoptóza MeSH
- cisplatina farmakologie MeSH
- DNA vazebné proteiny antagonisté a inhibitory metabolismus MeSH
- down regulace MeSH
- doxorubicin farmakologie MeSH
- G0 fáze MeSH
- inhibitory proteinkinas farmakologie MeSH
- lidé MeSH
- nádorové buněčné linie MeSH
- nádorové supresorové proteiny antagonisté a inhibitory metabolismus MeSH
- nádorový supresorový protein p53 metabolismus MeSH
- poškození DNA MeSH
- protein-serin-threoninkinasy antagonisté a inhibitory metabolismus MeSH
- proteiny buněčného cyklu antagonisté a inhibitory metabolismus MeSH
- průtoková cytometrie MeSH
- signální transdukce MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Cisplatin and doxorubicin are widely used anticancer drugs that cause DNA damage, which activates the ATM-Chk2-p53 pathway in cancer cells. This activation leads to cell cycle block or apoptosis, depending on the nature of the DNA damage. In an attempt to enhance the effects of these agents, we inhibited ATM/ATR and Chk2, which are known upstream regulators of p53. The cancer cell lines A2780 and ARN8, bearing the wild-type p53 protein, were used to study changes in p53 activation and trans-activation. Our results suggest that the G(1)-checkpoint, normally activated by DNA damage, is functionally overcome by the action of kinase inhibitors that sensitize cells to apoptosis. Both inhibitors show these effects, albeit with variable intensity in different cell lines, which is promising for other studies and theoretically for use in clinical practice.
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