ArticleOncotarget2016
Identification of H7 as a novel peroxiredoxin I inhibitor to induce differentiation of leukemia cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Mechanism-based peroxiredoxin 3 inhibitors exploit a covalent warhead for cancer therapy.Science advances · 2025Article
- Targeting PRDX1 impairs acute myeloid leukemic blasts and stem cells by disrupting redox homeostasis.Cell death & disease · 2025Article
- Discovery of novel and potent celastrol derivatives as PRDX1 inhibitors for cancer therapy through structure-based virtual screening.Frontiers in pharmacology · 2025Article
- Druggable upregulated proteins in EWS-FLI-driven Ewing sarcoma as emerging new therapeutic targets.American journal of translational research · 2025Review
- Article
- A Comprehensive Survey of Prospective Structure-Based Virtual Screening for Early Drug Discovery in the Past Fifteen Years.International journal of molecular sciences · 2022Review
- Genetic Inactivation of Peroxiredoxin-I Impairs the Growth of Human Pancreatic Cancer Cells.Antioxidants (Basel, Switzerland) · 2021Article
- Peroxiredoxins in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2020Review
- Peroxiredoxin Involvement in the Initiation and Progression of Human Cancer.Antioxidants & redox signaling · 2018Review
- CDDO-Me reveals USP7 as a novel target in ovarian cancer cells.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Identifying novel targets to enhance leukemia-cell differentiation is an urgent requirement. We have recently proposed that inhibiting the antioxidant enzyme peroxiredoxin I (Prdx I) may induce leukemia-cell differentiation. However, this concept remains to be confirmed. In this work, we identified H7 as a novel Prdx I inhibitor through virtual screening, in vitro activity assay, and surface plasmon resonance assay. Cellular thermal shift assay showed that H7 directly bound to Prdx I but not to Prdxs II-V in cells. H7 treatment also increased reactive oxygen species (ROS) level and cell differentiation in leukemia cells, as reflected by the upregulation of the cell surface differentiation marker CD11b/CD14 and the morphological maturation of cells. The differentiation-induction effect of H7 was further observed in some non-acute promyelocytic leukemia (APL) and primary leukemia cells apart from APL NB4 cells. Moreover, the ROS scavenger N-acetyl cysteine significantly reversed the H7-induced cell differentiation. We demonstrated as well that H7-induced cell differentiation was associated with the activation of the ROS-Erk1/2-C/EBPβ axis. Finally, we showed H7 treatment induced cell differentiation in an APL mouse model. All of these data confirmed that Prdx I was novel target for inducing leukemia-cell differentiation and that H7 was a novel lead compound for optimizing Prdx I inhibition.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.