ArticleJournal of biochemical and molecular toxicology2018
Trisenox induces cytotoxicity through phosphorylation of mitogen-activated protein kinase molecules in acute leukemia cells.
Article in Journal of biochemical and molecular toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Article
- Mechanistic update of Trisenox in blood cancer.Current research in pharmacology and drug discovery · 2023Review
- p53 as a unique target of action of cisplatin in acute leukaemia cells.Journal of cellular and molecular medicine · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Trisenox (TX) has been used successfully for the treatment of acute promyelocytic leukemia (APL) patients. TX-induced cytotoxicity in APL cells remains poorly understood. In this study, we investigated the molecular mechanism of TX cytotoxicity using APL cell lines. We assessed TX toxicity by quantitatively measuring lactate dehydrogenase levels. Inhibition of cell cycle progression was assessed by confocal microscopy of Ki-67 expression. Apoptosis was evaluated by Western blot analysis of apoptotic proteins expression, immunocytochemistry, and confocal imaging of annexin V and propidium iodide. Mitogen-activated protein kinase (MAPK) signaling cascade was analyzed by Western blot analysis and inhibitor-based experiments with APL cells. We found that TX-induced cytotoxicity inhibited APL cell cycle progression. TX also induced significant (P < 0.05) changes in the expression levels of apoptotic molecules and activated the phosphorylation of MAPK signaling pathways in APL cells. Understanding the mechanism of TX cytotoxicity would be helpful in the design of new APL drugs.
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Registered trials
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