Bredholt T 2009 Mol Cancer: Difference between revisions
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|title=Bredholt T, Dimba EA, Hagland HR, Wergeland L, Skavland J, Fossan KO, Tronstad KJ, Johannessen AC, Vintermyr OK, Gjertsen BT (2009) Camptothecin and khat (''Catha edulis'' Forsk.) induced distinct cell death phenotypes involving modulation of c-FLIPL, Mcl-1, procaspase-8 and mitochondrial function in acute myeloid leukemia cell lines. Mol Cancer 8: 101. | |title=Bredholt T, Dimba EA, Hagland HR, Wergeland L, Skavland J, Fossan KO, Tronstad KJ, Johannessen AC, Vintermyr OK, Gjertsen BT (2009) Camptothecin and khat (''Catha edulis'' Forsk.) induced distinct cell death phenotypes involving modulation of c-FLIPL, Mcl-1, procaspase-8 and mitochondrial function in acute myeloid leukemia cell lines. Mol Cancer 8:101. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19912650 PMID: 19912650] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/19912650 PMID: 19912650] | ||
|authors=Bredholt T, Dimba EA, Hagland HR, Wergeland L, Skavland J, Fossan KO, Tronstad KJ, Johannessen AC, Vintermyr OK, Gjertsen BT | |authors=Bredholt T, Dimba EA, Hagland HR, Wergeland L, Skavland J, Fossan KO, Tronstad KJ, Johannessen AC, Vintermyr OK, Gjertsen BT | ||
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|tissues=Blood cells | |tissues=Blood cells | ||
|preparations=Intact cells | |preparations=Intact cells | ||
|enzymes=Complex II; | |enzymes=Complex II;succinate dehydrogenase | ||
|injuries=Cell death | |injuries=Cell death | ||
|diseases=Cancer | |diseases=Cancer |
Revision as of 16:10, 17 February 2015
Bredholt T, Dimba EA, Hagland HR, Wergeland L, Skavland J, Fossan KO, Tronstad KJ, Johannessen AC, Vintermyr OK, Gjertsen BT (2009) Camptothecin and khat (Catha edulis Forsk.) induced distinct cell death phenotypes involving modulation of c-FLIPL, Mcl-1, procaspase-8 and mitochondrial function in acute myeloid leukemia cell lines. Mol Cancer 8:101. |
Bredholt T, Dimba EA, Hagland HR, Wergeland L, Skavland J, Fossan KO, Tronstad KJ, Johannessen AC, Vintermyr OK, Gjertsen BT (2009) Mol Cancer
Abstract: BACKGROUND: An organic extract of the recreational herb khat (Catha edulis Forsk.) triggers cell death in various leukemia cell lines in vitro. The chemotherapeutics camptothecin, a plant alkaloid topoisomerase I inhibitor, was tested side-by-side with khat in a panel of acute myeloid leukemia cell lines to elucidate mechanisms of toxicity.
RESULTS: Khat had a profound effect on MOLM-13 cells inducing mitochondrial damage, chromatin margination and morphological features of autophagy. The effects of khat on mitochondrial ultrastructure in MOLM-13 correlated with strongly impaired routine respiration, an effect neither found in the khat-resistant MV-4-11 cells nor in camptothecin treated cells. Enforced expression of anti-apoptotic Bcl-2 protein provided protection against camptothecin-induced cell death and partly against khat toxicity. Khat-induced cell death in MOLM-13 cells included reduced levels of anti-apoptotic Mcl-1 protein, while both khat and camptothecin induced c-FLIPL cleavage and procaspase-8 activation.
CONCLUSION: Khat activated a distinct cell death pathway in sensitive leukemic cells as compared to camptothecin, involving mitochondrial damage and morphological features of autophagy. This suggests that khat should be further explored in the search for novel experimental therapeutics. โข Keywords: Mitochondria, Oxidative phosphorilation, Programmed cell death, Camptothecin
โข O2k-Network Lab: NO Bergen Tronstad KJ
Labels: MiParea: Respiration, Genetic knockout;overexpression, Pharmacology;toxicology
Pathology: Cancer
Stress:Cell death
Organism: Human
Tissue;cell: Blood cells
Preparation: Intact cells
Enzyme: Complex II;succinate dehydrogenase
Regulation: ADP, Inhibitor
Coupling state: ROUTINE
HRR: Oxygraph-2k