ArticleHaematologica2017
Senescence is a Spi1-induced anti-proliferative mechanism in primary hematopoietic cells.
Article in Haematologica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 28 citations in OpenAlex.
- USP22 alleviates oxidative stress-induced BMSCs senescence by stabilizing SPI1 protein.Molecular genetics and genomics : MGG · 2026Article
- Comprehensive analysis of interactions between brain aging and late-onset psychoses using heuristic mapping models.Communications medicine · 2026Article
- DataXflowGen for GenAI-driven model generation.Scientific reports · 2026Article
- Exploiting cellular senescence in hematologic malignancies.Translational oncology · 2026Review
- USP7 sustains hematopoietic stem cell homeostasis partially via PU.1 stabilization.International journal of biological sciences · 2026Article
- Article
- Regulation of Hepatic Stellate Cell Phenotypes in Metabolic Dysfunction-Associated Steatohepatitis.Gastroenterology · 2025Review
- SPI1 activates mitochondrial unfolded response signaling to inhibit chondrocyte senescence and relieves osteoarthritis.Bone research · 2025Article
- Senescence-associated lineage-aberrant plasticity evokes T-cell-mediated tumor control.Nature communications · 2025Article
- Review
- Phenotypes and ontogeny of senescent hepatic stellate cells in metabolic dysfunction-associated steatohepatitis.Journal of hepatology · 2024Article
- FANCA deficiency promotes leukaemic progression by allowing the emergence of cells carrying oncogenic driver mutations.Oncogene · 2023Article
- Transcriptomic profiling reveals sex-specific molecular signatures of adipose endothelial cells under obesogenic conditions.iScience · 2023Article
- Identification of Metastasis-Associated Genes in Cutaneous Squamous Cell Carcinoma Based on Bioinformatics Analysis and Experimental Validation.Advances in therapy · 2022Article
- The ERK2-DBP domain opposes pathogenesis of a mouse JAK2V617F-driven myeloproliferative neoplasm.Blood · 2022Article
- Circulating primitive murine erythroblasts undergo complex proteomic and metabolomic changes during terminal maturation.Blood advances · 2022Article
- Overexpression of long non-coding RNA WT1-AS or silencing of PIK3AP1 are inhibitory to cervical cancer progression.Cell cycle (Georgetown, Tex.) · 2021Article
- The transcriptome of circulating cells indicates potential biomarkers and therapeutic targets in the course of hypertension-related myocardial infarction.Genes & diseases · 2021Article
- PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress.The Journal of experimental medicine · 2021Article
- Aging and pathological aging signatures of the brain: through the focusing lens of SIRT6.Aging · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.