ArticleMolecular cancer2009
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.
Article in Molecular cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Evaluation of Khat (Catha edulis) Use as a Risk Factor of Cancer: A Systematic Review.Asian Pacific journal of cancer prevention : APJCP · 2020Pooled it
- Impact of khat (Catha edulis) and oral contraceptive use on telomerase levels and tumor suppressor genes p53 and p21 in normal subjects and breast cancer patients.Scientific reports · 2024Article
- Phytochemicals and bioactive compounds effective against acute myeloid leukemia: A systematic review.Food science & nutrition · 2023Article
- The multifaceted roles of natural products in mitochondrial dysfunction.Frontiers in pharmacology · 2023Review
- Review
- Khat (Catha Edulis Forsk) induced apoptosis and cytotoxicity in cultured cells: A scoping review.Heliyon · 2021Article
- Qualitative ultrastructural analysis of the submandibular salivary glands after administration of khat: in vivo study.BMC research notes · 2021Article
- Progress and Research Trends onFrontiers in pharmacology · 2021Article
- Unraveling theFrontiers in pharmacology · 2021Article
- A Comparison of p53 Isoform Profiles and Apoptosis Induced by Camptothecin or a Herbal Khat Extract (Cancers · 2020Article
- Selaginellin B induces apoptosis and autophagy in pancreatic cancer cells via the JAK2/STAT3 signaling pathway.American journal of translational research · 2020Article
- T315 Decreases Acute Myeloid Leukemia Cell Viability through a Combination of Apoptosis Induction and Autophagic Cell Death.International journal of molecular sciences · 2016Article
- Article
- Catha edulis Extract Induces H9c2 Cell Apoptosis by Increasing Reactive Oxygen Species Generation and Activation of Mitochondrial Proteins.Pharmacognosy magazine · 2016Article
- Qat Chewing and Periodontal Pathogens in Health and Disease: Further Evidence for a Prebiotic-Like Effect.BioMed research international · 2015Article
- Poly(amido amine) dendrimers as absorption enhancers for oral delivery of camptothecin.International journal of pharmaceutics · 2013Article
- Reversible khat-induced hepatitis: two case reports and review of the literature.Frontline gastroenterology · 2013Article
- Distinct single cell signal transduction signatures in leukocyte subsets stimulated with khat extract, amphetamine-like cathinone, cathine or norephedrine.BMC pharmacology & toxicology · 2013Article
- Dual-acting histone deacetylase-topoisomerase I inhibitors.Bioorganic & medicinal chemistry letters · 2013Article
- Evaluation of the In Vitro Efficacy of Artemisia annua, Rumex abyssinicus, and Catha edulis Forsk Extracts in Cancer and Trypanosoma brucei Cells.ISRN biochemistry · 2013Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAn 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.
resultsKhat 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.
conclusionKhat 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.
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