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Senescence is a Spi1-induced anti-proliferative mechanism in primary hematopoietic cells
Open accessAbstract
Transcriptional deregulation caused by epigenetic or genetic alterations is a major cause of leukemic transformation. The Spi1/PU.1 transcription factor is a key regulator of many steps of hematopoiesis, and limits self-renewal of hematopoietic stem cells. The deregulation of its expression or activity contributes to leukemia, in which Spi1 can be either an oncogene or a tumor suppressor. Herein we explored whether cellular senescence, an anti-tumoral pathway that restrains cell proliferation, is a mechanism by which Spi1 limits hematopoietic cell expansion, and thus prevents the development of leukemia. We show that Spi1 overexpression triggers cellular senescence both in primary fibroblasts and hematopoietic cells. Erythroid and myeloid lineages are both prone to Spi1-induced senescence. In hematopoietic cells, Spi1-induced senescence requires its DNA-binding activity and a functional p38MAPK14 pathway but is independent of a DNA-damage response. In contrast, in fibroblasts, Spi1-induced senescence is triggered by a DNA-damage response. Importantly, using our well-established Spi1 transgenic leukemia mouse model, we demonstrate that Spi1 overexpression also induces senescence in erythroid progenitors of the bone marrow in vivo before the onset of the pre-leukemic phase of erythroleukemia. Remarkably, the senescence response is lost during the progression of the disease and erythroid blasts do not display a higher expression of Dec1 and CDKN1A, two of the induced senescence markers in young animals. These results bring indirect evidence that leukemia develops from cells which have bypassed Spi1-induced senescence. Overall, our results reveal senescence as a Spi1-induced anti-proliferative mechanism that may be a safeguard against the development of acute myeloid leukemia.
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PU.1 is commonly characterized as a lineage differentiation factor, and its role as a regulator of cell proliferation has also been extensively studied.
“while PU.1 is commonly characterized as a lineage differentiation factor, its role as a regulator of cell proliferation has also been extensively studied (Delestré et al., 2017; Fukuchi et al., 2008; Oikawa et al., 1999; Solomon et al., 2017; Ziliotto et al., 2014).”
From PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress (2021) · cites this paper as Delestré et al., 2017
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PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress
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Metadata
- Authors
- Delestré, L., Cui, H., Esposito, M., Quiveron, C., Mylonas, E., Penard-Lacronique, V., Bischof, O., & Guillouf, C.
- Affiliations
- Inserm (FR)
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Guillouf, Christel
- Venue
- Haematologica
- Published
- 2017-09-14
- Volume
- 102
- Issue
- 11
- Pages
- 1850-1860
- ISSN
- 0390-6078 (ISSN-L)
- 1592-8721
- PMC
- PMC5664389
- OpenAlex
- W2756263268
- Cited by
- 32
- References
- 50
- Citations by year
- 2026: 7 · 2025: 5 · 2024: 3 · 2023: 2 · 2022: 4 · 2021: 8 · 2020: 2 · 2019: 1
- FWCI
- 0.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Haematologica (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Institut Gustave-Roussy
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Keywords
- cellular senescence, antiproliferative mechanism, hematopoietic cells, acute myeloid leukemia, erythroid progenitor cells, erythroleukemia, p38 MAPK signaling, DNA damage response, leukemic transformation, DEC1, p21, transcription factor deregulation
- MeSH terms
- Ectopic Gene Expression, Proto-Oncogene Protein Spi-1, Animals, Bone Marrow, Cell Line, DNA-Binding Proteins, Fibroblasts, Hematopoietic Stem Cells, Humans, Immunohistochemistry, Leukemia, Mice, Transgenic, Mutation, Proto-Oncogene Proteins, Biomarkers, Trans-Activators, Cellular Senescence, Cell Proliferation, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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