Study of antitumor effect of selected vanadium and molybdenum organometallic complexes in human leukemic T-cells
Jazyk angličtina Země Irsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
26391003
DOI
10.1016/j.cbi.2015.09.017
PII: S0009-2797(15)30070-3
Knihovny.cz E-zdroje
- Klíčová slova
- Apoptosis, Jurkat, MOLT-4, Organometallic compounds, p53,
- MeSH
- apoptóza účinky léků MeSH
- fosforylace účinky léků MeSH
- kaspasy metabolismus MeSH
- leukemie T-buněčná farmakoterapie metabolismus patologie MeSH
- lidé MeSH
- molybden chemie farmakologie MeSH
- nádorové buněčné linie MeSH
- nádorový supresorový protein p53 metabolismus MeSH
- organokovové sloučeniny chemie farmakologie MeSH
- proliferace buněk účinky léků MeSH
- protinádorové látky farmakologie MeSH
- screeningové testy protinádorových léčiv MeSH
- serin metabolismus MeSH
- vanad chemie farmakologie MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- kaspasy MeSH
- molybden MeSH
- nádorový supresorový protein p53 MeSH
- organokovové sloučeniny MeSH
- protinádorové látky MeSH
- serin MeSH
- TP53 protein, human MeSH Prohlížeč
- vanad MeSH
This work describes cytotoxic effect of non-platinum metal-based compounds on the human T-leukemic cells with different p53 status (p53 wild-type MOLT-4 and p53-deficient Jurkat cells). The cytotoxic and apoptosis-inducing effect of the vanadium complex [(η(5)-C5H5)2V(5-NH2-phen)]OTf (V1) and molybdenum complex [(η(3)-C3H5)Mo(CO)2(phen)Cl] (Mo1) were studied using flow cytometry, spectrophotometry and Western blotting. We found that the cytotoxic effect of both tested complexes after 24 h is higher against the both examined cell lines than that of cis-platin (cis-DDP). At later investigated time intervals of 48 and 72 h, the cytotoxic effect of the cis-DDP increased but the values of the cytotoxicity of the tested V1 and Mo1 complexes remained unchanged, with the cytotoxicity of V1 comparable to that of cis-DDP. Furthermore we observed that the apoptotic process was induced by the activation of the caspases 9 (intrinsic pathway) and 8 (extrinsic pathway) in cells exposed to evaluated complexes. In case of the p53 wild-type MOLT-4 cells, the expression of the tumor-suppressor protein p53 and its form phosphorylated at the serine 15 increased after both V1 and Mo1 treatment, similar to the effect of cis-DDP.
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