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Inhibition of purom...
Inhibition of puromycin-induced apoptosis in breast cancer cells by IGF-I occurs simultaneously with increased protein synthesis
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Söderlund, Gustav (författare)
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- Haarhaus, Mathias, 1967- (författare)
- Östergötlands Läns Landsting,Linköpings universitet,Hälsouniversitetet,Njurmedicin,Njurmedicinska kliniken US
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- Chisalita, Ioana Simona, 1972- (författare)
- Linköpings universitet,Hälsouniversitetet,Avdelningen för medicinsk cellbiologi
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visa fler...
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- Arnqvist, Hans, 1943- (författare)
- Östergötlands Läns Landsting,Linköpings universitet,Hälsouniversitetet,Avdelningen för medicinsk cellbiologi,Endokrin- och magtarmmedicinska kliniken US
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visa färre...
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(creator_code:org_t)
- 2004
- 2004
- Engelska.
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Ingår i: Neoplasma (Bratislava). - 0028-2685 .- 1338-4317. ; 51:1
- Relaterad länk:
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https://urn.kb.se/re...
Abstract
Ämnesord
Stäng
- The objective of the following work was to study the apoptosis inducing effect of puromycin in MCF-7 breast cancer cells and compare this effect with cycloheximide and emetine, 2 other inhibitors of protein synthesis. We also wished to investigate if the apoptosis modulating effect of insulin-like growth factor-1 (IGF-I) was similar for the 3 inhibitors. An immunological assay, quantifying mono- and oligonucleosome fragments and morphological criteria after nuclear staining, were used to study apoptosis. Protein synthesis was measured by incorporation of 3H-leucine in the cells, and solution hybridization and Western blot were performed to estimate IGF-I receptor m-RNA and IGF-I receptor protein respectively. Puromycin at 0.5 μg/ml induced a high level of apoptosis in MCF-7 breast cancer cells, although there was still a non-negligible amount of synthesized protein. In the case of cycloheximide and emetine, apoptosis occured when protein synthesis was almost completely blocked. IGF-I at a concentration of 10 ng/ml significantly reduced the level of apoptosis induced by puromycin, emetine, or cycloheximide. We also noticed a parallel increase in 3H-leucine incorporation when apoptosis induced by puromycin was lowered as an effect of IGF-I, in contrast to cycloheximide and emetine where IGF-I reduced the apoptosis level without increasing the 3H-leucine incorporation. At a higher concentration of puromycin (5. 7 μg/ml), which blocked protein synthesis, IGF-I at 10 ng/ml did not reduce apoptosis. The level of IGF-I receptor m-RNA was not influenced by the use of a concentration of puromycin (0.5 μg/ml) inducing a high degree of apoptosis. These results suggest, that reduction of puromycin-induced apoptosis by IGF-I occurs simultaneously with increased protein synthesis, in contrast to emetine and cycloheximide. Furthermore it would appear that puromycin-induced apoptosis is not caused by reduced levels of IGF-I receptors.
Nyckelord
- MEDICINE
- MEDICIN
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