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Peloruside A-Induced Cell Death in Hypoxia Is p53 Dependent in HCT116 Colorectal Cancer Cells
J. Řehulka, N. Annadurai, I. Frydrych, P. Džubák, JH. Miller, M. Hajdúch, V. Das,
Journal of natural products.
2018 ;
81 (3) :
634-640.
[pub] 20180205
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
Perzistentní odkaz
https://www.medvik.cz/link/bmc19028592
- MeSH
- bicyklické sloučeniny heterocyklické farmakologie MeSH
- buněčná smrt účinky léků MeSH
- HCT116 buňky MeSH
- hypoxie farmakoterapie metabolismus MeSH
- inhibitor p21 cyklin-dependentní kinasy metabolismus MeSH
- kolorektální nádory farmakoterapie metabolismus MeSH
- laktony farmakologie MeSH
- lidé MeSH
- mikrotubuly účinky léků metabolismus MeSH
- nádorové buněčné linie MeSH
- nádorový supresorový protein p53 metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
HCT116 colorectal cancer cell sensitivity to peloruside A (PLA) in normoxia is not altered by hypoxia preconditioning of the cells. We examined whether the PLA effects were altered in hypoxia and whether the activity was dependent on p53. The cytotoxicity of PLA in wild-type HCT116 cells was largely unaffected by hypoxia; however, cells in which p53 was knocked out showed resistance. Knockout of the p21 gene had little effect on the activity of PLA in hypoxia. It was concluded that the response of cells to the microtubule-stabilizing agent PLA under hypoxic conditions is a p53-dependent process.
Citace poskytuje Crossref.org
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