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MicroRNAs 17-5p–20a–106a control monocytopoiesis through AML1 targeting and M-CSF receptor upregulation

Fontana, Laura, Pelosi, Elvira, Greco, Paolo, Racanicchi, Serena, Testa, Ugo, Liuzzi, Francesca, Croce, Carlo M., Brunetti, Ercole, Grignani, Francesco, Peschle, Cesare·2007·Nature Cell Biology
DOI 10.1038/ncb1613
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Abstract

We investigated the role of microRNAs (miRNA) 17-5p, 20a and 106a in monocytic differentiation and maturation. In unilineage monocytic culture generated by haematopoietic progenitor cells these miRNAs are downregulated, whereas the transcription factor acute myeloid leukaemia-1 (AML1; also known as Runt-related transcription factor 1, Runx1) is upregulated at protein but not mRNA level. As miRNAs 17-5p, 20a and 106a bind the AML1 mRNA 3'UTR, their decline may unblock AML1 translation. Accordingly, transfection with miRNA 17-5p-20a-106a suppresses AML1 protein expression, leading to M-CSF receptor (M-CSFR) downregulation, enhanced blast proliferation and inhibition of monocytic differentiation and maturation. Treatment with anti-miRNA 17-5p, 20a and 106a causes opposite effects. Knockdown of AML1 or M-CSFR by short interfering RNA (siRNA) mimics the action of the miRNA 17-5p-20a-106a, confirming that these miRNAs target AML1, which promotes M-CSFR transcription. In addition, AML1 binds the miRNA 17-5p-92 and 106a-92 cluster promoters and transcriptionally inhibits the expression of miRNA 17-5p-20a-106a. These studies indicate that monocytopoiesis is controlled by a circuitry involving sequentially miRNA 17-5p-20a-106a, AML1 and M-CSFR, whereby miRNA 17-5p-20a-106a function as a master gene complex interlinked with AML1 in a mutual negative feedback loop.

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  • Down-regulation of the miR-17p-92 cluster can promote myeloid lineage fate.

    “Furthermore, down-regulation of the miR-17p-92 cluster can promote myeloid lineage fate.13”

    From Macrophage development from HSCs requires PU.1-coordinated microRNA expression (2011) · cites this paper as [13]

  • Several miRs (e.g., miR-223 and the miR-17p-92 cluster) that were down-regulated by PU.1 have been shown to block macrophage differentiation.

    “In agreement with this, several of the miRs (eg, miR-223 and the miR-17p-92 cluster) that were down-regulated by PU.1 have been shown to block macrophage differentiation.10,13”

    From Macrophage development from HSCs requires PU.1-coordinated microRNA expression (2011) · cites this paper as [13]

Citations

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Metadata

Authors
Fontana, L., Pelosi, E., Greco, P., Racanicchi, S., Testa, U., Liuzzi, F., Croce, C. M., Brunetti, E., Grignani, F., & Peschle, C.
Venue
Nature Cell Biology
Publisher
Springer Science and Business Media LLC
Published
2007-06-24
Volume
9
Issue
7
Pages
775-787
ISSN
  • 1465-7392
  • 1476-4679
DOI
10.1038/ncb1613
Cited by
384
References
8
Language
en
Licence
www.springer.com/tdm (tdm)

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