The human nucleophosmin 1 mutation A inhibits myeloid differentiation of leukemia cells by modulating miR-10b

Oncotarget. 2016 Nov 1;7(44):71477-71490. doi: 10.18632/oncotarget.12216.

Abstract

Mutations in the nucleophosmin 1 (NPM1) gene are the most frequent genetic alteration in acute myeloid leukemia (AML). Here, we showed that enforced expression of NPM1 mutation type A (NPM1-mA) inhibits myeloid differentiation of leukemia cells, whereas knockdown of NPM1-mA has the opposite effect. Our analyses of normal karyotype AML samples from The Cancer Genome Atlas (TCGA) dataset revealed that miR-10b is commonly overexpressed in NPM1-mutated AMLs. We also found high expression of miR-10b in primary NPM1-mutated AML blasts and NPM1-mA positive OCI-AML3 cells. In addition, NPM1-mA knockdown enhanced myeloid differentiation, while induced expression of miR-10b reversed this effect. Finally, we showed that KLF4 is downregulated in NPM1-mutated AMLs. These results demonstrated that miR-10b exerts its effects by repressing the translation of KLF4 and that NPM1-mA inhibits myeloid differentiation through the miR-10b/KLF4 axis. This sheds new light on the effect of NPM1 mutations' on leukemogenesis.

Keywords: differentiation; leukemia; microRNA; mutation; nucleophosmin 1.

MeSH terms

  • Adult
  • Aged
  • Cell Differentiation
  • Female
  • HL-60 Cells
  • Humans
  • Kruppel-Like Factor 4
  • Kruppel-Like Transcription Factors / genetics
  • Leukemia, Myeloid, Acute / genetics
  • Leukemia, Myeloid, Acute / pathology*
  • Male
  • MicroRNAs / physiology*
  • Middle Aged
  • Mutation*
  • Nuclear Proteins / genetics*
  • Nucleophosmin
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • KLF4 protein, human
  • Kruppel-Like Factor 4
  • Kruppel-Like Transcription Factors
  • MIRN10 microRNA, human
  • MicroRNAs
  • NPM1 protein, human
  • Nuclear Proteins
  • Nucleophosmin
  • Tetradecanoylphorbol Acetate