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Anticancer efficiency of reovirus in normoxia and hypoxia
K. Figová, J. Hraběta, T. Eckschlager
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Free Medical Journals
od 2000
Freely Accessible Science Journals
od 2000
ProQuest Central
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2000
- MeSH
- apoptóza účinky léků MeSH
- autofagie účinky léků MeSH
- faktor 1 indukovatelný hypoxií - podjednotka alfa metabolismus MeSH
- fibroblasty účinky léků patologie virologie MeSH
- hypoxie buňky účinky léků MeSH
- kaspasa 3 metabolismus MeSH
- kyslík farmakologie MeSH
- lidé MeSH
- myši MeSH
- nádorové buněčné linie MeSH
- onkolytická viroterapie * MeSH
- onkolytické viry účinky léků fyziologie MeSH
- Reoviridae účinky léků fyziologie MeSH
- reovirové infekce patologie virologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Oncolytic viruses infect, replicate in, and lyse tumour cells but spare the normal ones. One of oncolytic viruses is a naturally occurring replication-competent reovirus (RV), which preferentially kills tumour cells with activated Ras signaling pathways. The aim of this study was to survey effects of RV on brain tumour-derived cells in vitro under hypoxic conditions since hypoxia causes resistance to radio- and chemotherapy. This study demonstrates that RV replicates preferentially in tumour cells and that the virus is able to overcome cellular adaptation to hypoxia and infect and kill hypoxic tumour cells. RV can both replicate in hypoxic tumour microenvironment and cause the cytopathic effect, subsequently inducing cell death. We found that a large proportion of cells are killed in hypoxia (1% O₂) by caspase-independent mechanisms. Furthermore, we learned that the cell death induced by RV in hypoxic conditions is not caused by autophagy.
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