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• W2254925724 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." @default.
• W2254925724 created "2016-06-24" @default.
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• W2254925724 date "2015-12-26" @default.
• W2254925724 modified "2023-10-16" @default.
• W2254925724 title "Identification of H7 as a novel peroxiredoxin I inhibitor to induce differentiation of leukemia cells" @default.
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• W2254925724 doi "https://doi.org/10.18632/oncotarget.6763" @default.
• W2254925724 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4826176" @default.
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