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Cytotoxicity and mitochondrial apoptosis induced by etoposide in melanoma cells
K. Rudolf, M. Červinka, E. Rudolf
Cancer investigation.
2009 ;
27 (7) :
704-717.
Language English Country Great Britain
Document type Research Support, Non-U.S. Gov't
Persistent link
https://www.medvik.cz/link/bmc11016718
NLK
Medline Complete (EBSCOhost)
from 2001-01-01 to 1 year ago
- MeSH
- Adenosine Triphosphate metabolism MeSH
- Apoptosis drug effects MeSH
- Benzothiazoles pharmacology MeSH
- Cyclosporine pharmacology MeSH
- Cysteine Endopeptidases metabolism MeSH
- DNA-Binding Proteins antagonists & inhibitors metabolism MeSH
- Etoposide pharmacology MeSH
- Antineoplastic Agents, Phytogenic pharmacology MeSH
- Cysteine Proteinase Inhibitors pharmacology MeSH
- Caspase Inhibitors MeSH
- Protein Kinase Inhibitors pharmacology MeSH
- Caspase 2 metabolism MeSH
- Caspase 3 metabolism MeSH
- Caspase 9 metabolism MeSH
- Humans MeSH
- Melanoma pathology MeSH
- Mitochondria drug effects MeSH
- Tumor Cells, Cultured drug effects MeSH
- Neoplasm Proteins antagonists & inhibitors metabolism MeSH
- Tumor Suppressor Proteins antagonists & inhibitors metabolism MeSH
- Tumor Suppressor Protein p53 metabolism MeSH
- DNA Damage MeSH
- bcl-2-Associated X Protein metabolism MeSH
- Protein Serine-Threonine Kinases antagonists & inhibitors metabolism MeSH
- Cell Cycle Proteins metabolism MeSH
- Superoxides metabolism MeSH
- Toluene analogs & derivatives pharmacology MeSH
- Check Tag
- Humans MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
Cytotoxicity and apoptosis induced by etoposide were studied during 72 hr in human melanoma cells. Etoposide initiated DNA-damage signaling via ATM kinase and activated p53 pathway and caspase-2. In response to treatment with etoposide, mitochondria of melanoma cells first increased their abundance and activity, and at later treatment intervals their dynamic behavior and functions became suppressed. Observed mitochondrial perturbation was not preceded by membrane potential loss but cytochrome c release was observed together with a rise in caspase-9 and caspase-3 activities. The pharmacological inhibition of relevant induced targets proved the importance of ATM and caspase-2 in etoposide-mediated cytotoxicity and apoptosis.
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