ArticlePloS one2012
Spi-1, Fli-1 and Fli-3 (miR-17-92) oncogenes contribute to a single oncogenic network controlling cell proliferation in friend erythroleukemia.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- A Novel FLI1 Monoclonal Antibody Which Recognizes EWS::FLI1 with High Affinity Is Useful for Detecting Ewing Sarcoma.Antibodies (Basel, Switzerland) · 2025Article
- Circulating Exosomes from Septic Mice Activate NF-κB/MIR17HG Pathway in Macrophages.Biomedicines · 2024Article
- STAT3 and SPI1, may lead to the immune system dysregulation and heterotopic ossification in ankylosing spondylitis.BMC immunology · 2022Article
- miR-17-92 cluster in osteoarthritis: Regulatory roles and clinical utility.Frontiers in genetics · 2022Review
- The transcription factor TAL1 and miR-17-92 create a regulatory loop in hematopoiesis.Scientific reports · 2020Article
- The HMG box transcription factor HBP1: a cell cycle inhibitor at the crossroads of cancer signaling pathways.Cellular and molecular life sciences : CMLS · 2019Review
- The Wnt/β-Catenin/LEF1 Pathway Promotes Cell Proliferation at Least in Part Through Direct Upregulation of miR-17-92 Cluster.Frontiers in genetics · 2019Article
- Differential Sensitivity of Target Genes to Translational Repression by miR-17~92.PLoS genetics · 2017Article
- Article
- VEGF-Induced Expression of miR-17-92 Cluster in Endothelial Cells Is Mediated by ERK/ELK1 Activation and Regulates Angiogenesis.Circulation research · 2016Article
- The MYC/miR-17-92 axis in lymphoproliferative disorders: A common pathway with therapeutic potential.Oncotarget · 2015Review
- Epigenetic silencing of Bim transcription by Spi-1/PU.1 promotes apoptosis resistance in leukaemia.Cell death and differentiation · 2013Article
- mir-17-92: a polycistronic oncomir with pleiotropic functions.Immunological reviews · 2013Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clonal erythroleukemia developing in susceptible mice infected by Friend virus complex are associated with highly recurrent proviral insertions at one of three loci called Spi-1, Fli-1 or Fli-3, leading to deregulated expression of oncogenic Spi-1 or Fli-1 transcription factors or miR-17-92 miRNA cluster, respectively. Deregulated expression of each of these three oncogenes has been independently shown to contribute to cell proliferation of erythroleukemic clones. Previous studies showed a close relationship between Spi-1 and Fli-1, which belong to the same ETS family, Spi-1 activating fli-1 gene, and both Spi-1 and Fli-1 activating multiple common target genes involved in ribosome biogenesis. In this study, we demonstrated that Spi-1 and Fli-1 are also involved in direct miR-17-92 transcriptional activation through their binding to a conserved ETS binding site in its promoter. Moreover, we demonstrated that physiological re-expression of exogenous miR-17 and miR-20a are able to partially rescue the proliferation loss induced by Fli-1 knock-down and identified HBP1 as a target of these miRNA in erythroleukemic cells. These results establish that three of the most recurrently activated oncogenes in Friend erythroleukemia are actually involved in a same oncogenic network controlling cell proliferation. The putative contribution of a similar ETS-miR-17-92 network module in other normal or pathological proliferative contexts is discussed.
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