ArticleCancer research2008
BMI-1 promotes ewing sarcoma tumorigenicity independent of CDKN2A repression.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02404480 (A Phase 1 Study of PTC596 in Patients With Advanced Solid Tumors), which is not on this map. Cited by 83 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Phase 1 Study of PTC596 in Patients With Advanced Solid Tumors
Who cites it
83 citing papers in PubMed, 129 citations in OpenAlex.
- Targeting autophagy and metabolism for ewing sarcoma.Molecular biology reports · 2025Review
- JMJD3-mediated senescence is required to overcome stress-induced hematopoietic defects.EMBO reports · 2025Article
- Polycomb protein Bmi1 promotes odontoblast differentiation by accelerating Wnt and BMP signaling pathways.Histochemistry and cell biology · 2024Article
- Critical Differential Expression Assessment for Individual Bulk RNA-Seq Projects.bioRxiv : the preprint server for biology · 2024Article
- PP2A inhibitor SET promotes mTORC1 and Bmi1 signaling through Akt activation and maintains the colony-formation ability of cancer cells.The Journal of biological chemistry · 2024Article
- BMI1 is required for melanocyte stem cell maintenance and hair pigmentation.Pigment cell & melanoma research · 2023Article
- Targeting BMI-1 in B cells restores effective humoral immune responses and controls chronic viral infection.Nature immunology · 2022Article
- Epigenetic regulator BMI1 promotes alveolar rhabdomyosarcoma proliferation and constitutes a novel therapeutic target.Molecular oncology · 2021Article
- Article
- BMI-1 Expression Heterogeneity in Endometriosis-Related and Non-Endometriotic Ovarian Carcinoma.International journal of molecular sciences · 2021Article
- Article
- Senescence Induced by BMI1 Inhibition Is a Therapeutic Vulnerability in H3K27M-Mutant DIPG.Cell reports · 2020Article
- RING1B recruits EWSR1-FLI1 and cooperates in the remodeling of chromatin necessary for Ewing sarcoma tumorigenesis.Science advances · 2020Article
- Review
- Review
- Article
- Epigenetic Regulation and Dietary Control of Triple Negative Breast Cancer.Frontiers in nutrition · 2020Review
- Aberrantly elevated Bmi1 promotes cervical cancer tumorigenicity and tumor sphere formation via enhanced transcriptional regulation of Sox2 genes.Oncology reports · 2019Article
- Anatomic Origin of Osteochondrogenic Progenitors Impacts Sensitivity to EWS-FLI1-Induced Transformation.Cancers · 2019Article
- ASXL2 regulates hematopoiesis in mice and its deficiency promotes myeloid expansion.Haematologica · 2018Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Deregulation of the polycomb group gene BMI-1 is implicated in the pathogenesis of many human cancers. In this study, we have investigated if the Ewing sarcoma family of tumors (ESFT) expresses BMI-1 and whether it functions as an oncogene in this highly aggressive group of bone and soft tissue tumors. Our data show that BMI-1 is highly expressed by ESFT cells and that, although it does not significantly affect proliferation or survival, BMI-1 actively promotes anchorage-independent growth in vitro and tumorigenicity in vivo. Moreover, we find that BMI-1 promotes the tumorigenicity of both p16 wild-type and p16-null cell lines, demonstrating that the mechanism of BMI-1 oncogenic function in ESFT is, at least in part, independent of CDKN2A repression. Expression profiling studies of ESFT cells following BMI-1 knockdown reveal that BMI-1 regulates the expression of hundreds of downstream target genes including, in particular, genes involved in both differentiation and development as well as cell-cell and cell-matrix adhesion. Gain and loss of function assays confirm that BMI-1 represses the expression of the adhesion-associated basement membrane protein nidogen 1. In addition, although BMI-1 promotes ESFT adhesion, nidogen 1 inhibits cellular adhesion in vitro. Together, these data support a pivotal role for BMI-1 ESFT pathogenesis and suggest that its oncogenic function in these tumors is in part mediated through modulation of adhesion pathways.
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Registered trials
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.