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Mechanism of action...
Mechanism of action for N-substituted benzamide-induced apoptosis.
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Olsson, A R (författare)
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- Lindgren, Hanna (författare)
- Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups
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- Pero, Ronald (författare)
- Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups
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visa fler...
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- Leanderson, Tomas (författare)
- Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups
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(creator_code:org_t)
- 2002
- 2002
- Engelska.
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Ingår i: British Journal of Cancer. - 1532-1827. ; 86:6, s. 971-978
- Relaterad länk:
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http://www.ncbi.nlm....
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visa fler...
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http://dx.doi.org/10...
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https://lup.lub.lu.s...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- We have analysed the mechanism of action for induction of apoptosis by N-substituted benzamides using declopramide as a lead compound. We show here that declopramide at doses above 250 microM in the mouse 70Z/3 pre-B cell line or in the human promyeolocytic cancer cell line HL60 induced cytochrome c release into the cytosol and caspase-9 activation. The broad spectrum caspase inhibitor zVADfmk and caspase-9 inhibitor zLEDHfmk inhibited apoptosis and improved cell viability when administrated to cells 1 h before exposure to declopramide, whereas the caspase-8 inhibitor zIEDHfmk had less effect. Also, the over expression of Bcl-2 by transfection in 70Z/3 cells inhibited declopramide-induced apoptosis. Prior to the induction of apoptosis, a G(2)/M cell cycle block was induced by declopramide. The cell cycle block was also observed in the presence of broad spectrum caspase inhibitor zVADfmk and in a transfectant expressing high levels of Bcl-2. Furthermore, while p53 was induced in 70Z/3 cells by declopramide, neither the apoptotic mechanism nor the G(2)/M cell cycle block were dependent on p53 activation since both effects were also seen in p53 deficient HL60 cells after addition of declopramide.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Cancer och onkologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Cancer and Oncology (hsv//eng)
Nyckelord
- G2 Phase : drug effects
- HL-60 Cells
- Metoclopramide : pharmacology
- Human
- Mitosis : drug effects
- Procainamide : analogs & derivatives
- Procainamide : pharmacology
- Protein p53 : physiology
- Benzamides : pharmacology
- Proto-Oncogene Proteins c-bcl-2 : physiology
- Cytochrome c : secretion
- Enzyme Activation
- Apoptosis : drug effects
- Caspases : metabolism
Publikations- och innehållstyp
- art (ämneskategori)
- ref (ämneskategori)
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