ArticleCancer biology & therapy2013
Regulation of the kinase RSK1 by arsenic trioxide and generation of antileukemic responses.
Article in Cancer biology & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Mechanistic update of Trisenox in blood cancer.Current research in pharmacology and drug discovery · 2023Review
- RSK Isoforms in Acute Myeloid Leukemia.Biomedicines · 2021Review
- Direct binding of arsenic trioxide to AMPK and generation of inhibitory effects on acute myeloid leukemia precursors.Molecular cancer therapeutics · 2015Article
- Hyperoside enhances the suppressive effects of arsenic trioxide on acute myeloid leukemia cells.International journal of clinical and experimental medicine · 2015Article
- Resveratrol enhances the suppressive effects of arsenic trioxide on primitive leukemic progenitors.Cancer biology & therapy · 2014Article
- Arsenic in leukemia: a RSKy business.Cancer biology & therapy · 2013Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Arsenic Trioxide (As₂O₃) is one of the most effective agents in the treatment of acute promyelocytic leukemia (APL), but has no significant efficacy in other forms of AML. The mechanisms of relative resistance of non-APL cells are not well understood, but emerging evidence suggests that activation of negative feedback regulatory loops and pathways contributes to such resistance. We provide evidence that a signaling cascade involving the kinase RSK1 is engaged in a negative feedback manner during arsenic-treatment of cells and exhibits regulatory effects on growth and survival of AML cells in response to treatment with As₂O₃. Our data demonstrate that pharmacological inhibition or molecular disruption of expression of RSK1 enhances As₂O₃-dependent apoptosis and/or growth inhibition of AML cells. Importantly, combination of a pharmacological inhibitor of RSK and As₂O₃ results in enhanced suppression of primary AML leukemic progenitors. Altogether, our findings suggest an important regulatory role for RSK1 in the generation of the effects of As₂O₃ in AML cells. They also raise the potential of RSK1 targeting in combination with As₂O₃ as a novel approach to promote antileukemic responses.
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Registered trials
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