ArticleLeukemia2012
E2F4 plays a key role in Burkitt lymphoma tumorigenesis.
Article in Leukemia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Transcription factor E2F4 facilitates SUMOylation to promote HCC progression through interaction with LIN9.International journal of oncology · 2024Article
- Glutathione overproduction mediates lymphoma initiating cells survival and has a sex-dependent effect on lymphomagenesis.Cell death & disease · 2024Article
- Methylation silencing CDH23 is a poor prognostic marker in diffuse large B-cell lymphoma.Aging · 2021Article
- Transcription factor E2F4 is an indicator of poor prognosis and is related to immune infiltration in hepatocellular carcinoma.Journal of Cancer · 2021Article
- LncRNA HAND2-AS1 represses cervical cancer progression by interaction with transcription factor E2F4 at the promoter of C16orf74.Journal of cellular and molecular medicine · 2020Article
- CDCA7 finely tunes cytoskeleton dynamics to promote lymphoma migration and invasion.Haematologica · 2020Article
- DNA methylation profiles in chronic lymphocytic leukemia patients treated with chemoimmunotherapy.Clinical epigenetics · 2019Article
- CDCA7 is a critical mediator of lymphomagenesis that selectively regulates anchorage-independent growth.Haematologica · 2018Article
- MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter.Nucleic acids research · 2017Article
- Integrative Genomic Analyses Yield Cell-Cycle Regulatory Programs with Prognostic Value.Molecular cancer research : MCR · 2016Article
- Epigenomic evolution in diffuse large B-cell lymphomas.Nature communications · 2015Article
- REACTIN: regulatory activity inference of transcription factors underlying human diseases with application to breast cancer.BMC genomics · 2013Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sporadic Burkitt lymphoma (sBL) is a rapidly growing B-cell non-Hodgkin's lymphoma whose treatment requires highly aggressive therapies that often result severely toxic. Identification of proteins whose expression or function is deregulated in sBL and play a role in its formation could facilitate development of less toxic therapies. We have previously shown that E2F1 expression is deregulated in sBL. We have now investigated the mechanisms underlying E2F1 deregulation and found that the E2F sites in its promoter fail to repress its transcriptional activity in BL cells and that the transcriptional repressor E2F4 barely interacts with these sites. We also have found that E2F4 protein levels, but not those of its mRNA, are reduced in sBL cell lines relative to immortal B-cell lines. E2F4 protein expression is also decreased in 24 of 26 sBL tumor samples from patients compared with control tissues. Our data demonstrate that enforced E2F4 expression in BL cells not only diminishes E2F1 levels, but also reduces selectively the tumorigenic properties and proliferation of BL cells, while increasing their accumulation in G(2)/M. Our results therefore point to E2F4 as a target for developing novel and less toxic treatments for sBL.
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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.