ArticleJournal of Cancer2020
Arsenic trioxide induces autophagic degradation of the FLT3-ITD mutated protein in FLT3-ITD acute myeloid leukemia cells.
Article in Journal of Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- A global bibliometric and visualized analysis of the links between the autophagy and acute myeloid leukemia.Frontiers in pharmacology · 2023Pooled it
- Long-term outcome of children with acute promyelocytic leukemia: a randomized study of oral versus intravenous arsenic by SCCLG-APL group.Blood cancer journal · 2023Trial
- Autophagy and Lipid Metabolism as a Therapeutic Target for Overcoming Drug Resistance in Acute Myeloid Leukemia.Life (Basel, Switzerland) · 2026Review
- Inhibition of NRF2 signaling overcomes acquired resistance to arsenic trioxide in FLT3-mutated Acute Myeloid Leukemia.Annals of hematology · 2024Article
- The genomic landscape of sensitivity to arsenic trioxide uncovered by genome-wide CRISPR-Cas9 screening.Frontiers in oncology · 2023Article
- Curcumin combined with arsenic trioxide in the treatment of acute myeloid leukemia: network pharmacology analysis and experimental validation.Journal of cancer research and clinical oncology · 2023Article
- Mechanistic update of Trisenox in blood cancer.Current research in pharmacology and drug discovery · 2023Review
- A bavachinin analog, D36, induces cell death by targeting both autophagy and apoptosis pathway in acute myeloid leukemia cells.Cancer chemotherapy and pharmacology · 2022Article
- Therapeutic Targeting of FLT3 in Acute Myeloid Leukemia: Current Status and Novel Approaches.OncoTargets and therapy · 2022Review
- Review
- Autophagy a Close Relative of AML Biology.Biology · 2021Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prognosis of acute myeloid leukemia (AML) with FMS-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD) mutations is poor. Some studies, including our previous study, have indicated that arsenic trioxide (ATO) exhibited significant anti-carcinogenic activity in FLT3-ITD AML cells and explored the possibility of targeting the FLT3-ITD protein for degradation as a therapy. Autophagy is a critical mechanism of the anti-leukemic effects of ATO. In this study, we explored the therapeutic efficacy of ATO treatment in a mouse model bearing FLT3-ITD AML and found that ATO significantly reduced the leukemic burden in bone marrow and spleen. We also found that autophagy was responsible for, at least in part, the degradation of the FLT3-ITD protein by ATO. After ATO treatment, MV4-11 cells showed complete autophagic flux. The autophagy inhibitor bafilomycin A or down-regulation of the key autophagy genes Atg5 and Atg7 reversed the FLT3 degradation induced by ATO. We also found that p62/SQSTM1 delivered FLT3-ITD proteins to the lysosome, where they were subsequently degraded. These results indicate that ATO can induce autophagic degradation of the FLT3-ITD mutated protein in FLT3-ITD AML.
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Registered trials
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