ArticleOncogene2004
Role of protein-protein interactions in the antiapoptotic function of EWS-Fli-1.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Mechanism of action and treatment of type I interferon in hepatocellular carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
- Non-chemotherapy adjuvant agents in TP53 mutant Ewing sarcoma.Scientific reports · 2023Article
- Targeted Therapy for EWS-FLI1 in Ewing Sarcoma.Cancers · 2023Review
- ETV6 dependency in Ewing sarcoma by antagonism of EWS-FLI1-mediated enhancer activation.Nature cell biology · 2023Article
- SPOP and OTUD7A Control EWS-FLI1 Protein Stability to Govern Ewing Sarcoma Growth.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Development of an Ewing sarcoma cell line with resistance to EWS‑FLI1 inhibitor YK‑4‑279.Molecular medicine reports · 2020Article
- Identifying the druggable interactome of EWS-FLI1 reveals MCL-1 dependent differential sensitivities of Ewing sarcoma cells to apoptosis inducers.Oncotarget · 2018Article
- Review
- Molecular Mechanism ofJournal of pharmaceutical sciences and pharmacology · 2015Article
- EWS/FLI utilizes NKX2-2 to repress mesenchymal features of Ewing sarcoma.Genes & cancer · 2015Article
- EWS-FLI1 utilizes divergent chromatin remodeling mechanisms to directly activate or repress enhancer elements in Ewing sarcoma.Cancer cell · 2014Article
- Anti-Epileptic Drug Targets Ewing Sarcoma.Journal of pharmaceutical sciences and pharmacology · 2014Article
- Mechanism and relevance of EWS/FLI-mediated transcriptional repression in Ewing sarcoma.Oncogene · 2013Article
- Molecular pathogenesis of Ewing sarcoma: new therapeutic and transcriptional targets.Annual review of pathology · 2012Review
- Regulation of endothelial cell development by ETS transcription factors.Seminars in cell & developmental biology · 2011Review
- Histone deacetylase inhibitors, valproic acid and trichostatin-A induce apoptosis and affect acetylation status of p53 in ERG-positive prostate cancer cells.International journal of oncology · 2011Article
- Ecteinascidin 743 interferes with the activity of EWS-FLI1 in Ewing sarcoma cells.Neoplasia (New York, N.Y.) · 2011Article
- Factors Affecting EWS-FLI1 Activity in Ewing's Sarcoma.Sarcoma · 2011Article
- Article
- Oncogenic partnerships: EWS-FLI1 protein interactions initiate key pathways of Ewing's sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
In the majority of Ewing's family tumors, chromosomal translocation t(11;22) leads to aberrant fusion of RNA-binding protein EWS with DNA-binding ETS transcriptional factor Fli-1. EWS-Fli-1 has altered the transcriptional activity and modulating its downstream target genes through this transcriptional activity is thought to be responsible for this tumor. We have previously shown that both EWS-Fli-1 and Fli-1 have antiapoptotic activity against several apoptotic inducers. Here, we show that the transcriptional activity of EWS-Fli-1 and Fli-1 is not essential for its antiapoptotic activity. We also demonstrate that EWS-Fli-1 and Fli-1 interact with CBP through its amino-terminal region and inhibit the CBP-dependent transcriptional activity of RXR. This activity appears to be independent of DNA-binding activity of EWS-Fli-1. Introduction of the dominant-negative form of CBP into Ewing's sarcoma cells sensitizes these cells against genotoxic or retinoic-acid induced apoptosis. These results suggest that the ability of EWS-Fli-1/Fli-1 to target transcriptional cofactor(s) and modulate apoptotic pathways may be responsible for its antiapoptotic and tumorigenic activities.
Indexed as
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What OpenQuestion holds
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.