ArticleMolecular and cellular biology2012
Transcriptional regulation of the human tumor suppressor DOK1 by E2F1.
Article in Molecular and cellular biology, 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, 18 citations in OpenAlex.
- Comprehensive analysis of DOK family genes expression, immune characteristics, and drug sensitivity in human tumors.Journal of advanced research · 2022Article
- Docking protein 1 and free fatty acids are associated with insulin resistance in patients with type 2 diabetes mellitus.The Journal of international medical research · 2021Article
- Disease-related cellular protein networks differentially affected under different EGFR mutations in lung adenocarcinoma.Scientific reports · 2020Article
- Methylation-associated DOK1 and DOK2 down-regulation: Potential biomarkers for predicting adverse prognosis in acute myeloid leukemia.Journal of cellular physiology · 2018Article
- lncRNA-HIT promotes cell proliferation of non-small cell lung cancer by association with E2F1.Cancer gene therapy · 2017Article
- mRNA and methylation profiling of radioresistant esophageal cancer cells: the involvement of Sall2 in acquired aggressive phenotypes.Journal of Cancer · 2017Article
- Subcellular compartmentalization of docking protein-1 contributes to progression in colorectal cancer.EBioMedicine · 2016Article
- Dimeric switch of Hakai-truncated monomers during substrate recognition: insights from solution studies and NMR structure.The Journal of biological chemistry · 2014Article
- eIF2α dephosphorylation in basolateral amygdala mediates reconsolidation of drug memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Epstein-Barr virus down-regulates tumor suppressor DOK1 expression.PLoS pathogens · 2014Article
- EgoNet: identification of human disease ego-network modules.BMC genomics · 2014Article
- BRK targets Dok1 for ubiquitin-mediated proteasomal degradation to promote cell proliferation and migration.PloS one · 2014Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of the tumor suppressor DOK1 is repressed in a variety of human tumors as a result of hypermethylation of its promoter region. However, the molecular mechanisms by which DOK1 expression is regulated have been poorly investigated. Here, we show that the expression of DOK1 is regulated mainly by the transcription factor E2F1. We identified three putative E2F1 response elements (EREs) in the DOK1 promoter region. E2F1 had a relatively higher binding affinity for the ERE located between bp -498 and -486 compared with the other two EREs. E2F1 gene silencing strongly inhibited DOK1 expression. E2F1-driven DOK1 transcription occurred in the presence of cellular stresses, such as accumulation of DNA damage induced by etoposide. DOK1 silencing promoted cell proliferation and protected against etoposide-induced apoptosis, indicating that DOK1 acts as a key mediator of cellular stress-induced cell death. Most importantly, we observed that DNA methylation of the DOK1 core promoter region found in head and neck cancer cell lines hampered the recruitment of E2F1 to the DOK1 promoter and compromised DOK1 expression. In summary, our data show that E2F1 is a key factor in DOK1 expression and provide novel insights into the regulation of these events in cancer cells.
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