ArticleBMC molecular biology2008
Transcriptional regulation of BRD7 expression by Sp1 and c-Myc.
Article in BMC molecular biology, 2008. 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, 36 citations in OpenAlex.
- Integrative multi-omic analysis identifies key transcription factors and target proteins in renal cell carcinoma and its subtypes.bioRxiv : the preprint server for biology · 2025Article
- TRIM28 promotes tumor growth and metastasis in breast cancer by targeting the BRD7 protein for ubiquitination and degradation.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Interaction and Collaboration of SP1, HIF-1, and MYC in Regulating the Expression of Cancer-Related Genes to Further Enhance Anticancer Drug Development.Current issues in molecular biology · 2023Review
- Targeting Myc Interacting Proteins as a Winding Path in Cancer Therapy.Frontiers in pharmacology · 2021Review
- Zinc-finger protein YY1 suppresses tumor growth of human nasopharyngeal carcinoma by inactivating c-Myc-mediatedThe Journal of biological chemistry · 2019Article
- Bromodomain‑containing protein 7 sensitizes breast cancer cells to paclitaxel by activating Bcl2‑antagonist/killer protein.Oncology reports · 2019Article
- BRD7 expression and c-Myc activation forms a double-negative feedback loop that controls the cell proliferation and tumor growth of nasopharyngeal carcinoma by targeting oncogenic miR-141.Journal of experimental & clinical cancer research : CR · 2018Article
- Article
- Tumor suppressor bromodomain-containing protein 7 cooperates with Smads to promote transforming growth factor-β responses.Oncogene · 2017Article
- MiR-200c is a cMyc-activated miRNA that promotes nasopharyngeal carcinoma by downregulating PTEN.Oncotarget · 2017Article
- Loss of TINCR expression promotes proliferation, metastasis through activating EpCAM cleavage in colorectal cancer.Oncotarget · 2016Article
- Bromodomain-containing protein 7 (BRD7) as a potential tumor suppressor in hepatocellular carcinoma.Oncotarget · 2016Article
- miR-141 is involved in BRD7-mediated cell proliferation and tumor formation through suppression of the PTEN/AKT pathway in nasopharyngeal carcinoma.Cell death & disease · 2016Article
- Knockout of BRD7 results in impaired spermatogenesis and male infertility.Scientific reports · 2016Article
- Integrating ChIP-sequencing and digital gene expression profiling to identify BRD7 downstream genes and construct their regulating network.Molecular and cellular biochemistry · 2016Article
- BRD7 Acts as a Tumor Suppressor Gene in Lung Adenocarcinoma.PloS one · 2016Article
- BRD7: a novel tumor suppressor gene in different cancers.American journal of translational research · 2016Review
- Disturbing miR-182 and -381 inhibits BRD7 transcription and glioma growth by directly targeting LRRC4.PloS one · 2014Article
- Site-specific chromatin immunoprecipitation: a selective method to individually analyze neighboring transcription factor binding sites in vivo.BMC research notes · 2012Article
- Identification of cis-Regulatory Elements in the dmyc Gene of Drosophila Melanogaster.Gene regulation and systems biology · 2012Article
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBromodomain is an evolutionally conserved domain that is found in proteins strongly implicated in signal-dependent transcriptional regulation. Genetic alterations of bromodomain genes contributed to the development of many human cancers and other disorders. BRD7 is a recently identified bromodomain gene. It plays a critical role in cellular growth, cell cycle progression, and signal-dependent gene expression. Previous studies showed that BRD7 gene exhibited much higher-level of mRNA expression in normal nasopharyngeal epithelia than in nasopharyngeal carcinoma (NPC) biopsies and cell lines. However, little is known about its transcriptional regulation. In this study, we explored the transcriptional regulation of BRD7 gene.
methodPotential binding sites of transcription factors within the promoter region of BRD7 gene were predicted with MatInspector Professional http://genomatix.de/cgi-bin/matinspector_prof/mat_fam.pl. Mutation construct methods and luciferase assays were performed to define the minimal promoter of BRD7 gene. RT-PCR and western blot assays were used to detect the endogenous expression of transcription factor Sp1, c-Myc and E2F6 in all cell lines used in this study. Electrophoretic mobility shift assays (EMSA) and Chromatin immunoprecipitation (ChIP) were used to detect the direct transcription factors that are responsible for the promoter activity of BRD7 gene. DNA vector-based siRNA technology and cell transfection methods were employed to establish clone pools that stably expresses SiRNA against c-Myc expression in nasopharyngeal carcinoma 5-8F cells. Real-time PCR was used to detect mRNA expression of BRD7 gene in 5-8F/Si-c-Myc cells.
resultsWe defined the minimal promoter of BRD7 gene in a 55-bp region (from -266 to -212bp), and identified that its promoter activity is inversely related to c-Myc expression. Sp1 binds to the Sp1/Myc-Max overlapping site of BRD7 minimal promoter, and slightly positively regulate its promoter activity. c-Myc binds to this Sp1/Myc-Max overlapping site as well, and negatively regulates the promoter activity and endogenous mRNA expression of BRD7 gene. Knock-down of c-Myc increases the promoter activity and mRNA level of BRD7 gene. The luciferase activity of the mutated promoter constructs showed that Sp1/Myc-Max overlapping site is a positive regulation element of BRD7 promoter.
conclusionThese studies provide for the first time the evidence that c-Myc is indeed a negative regulator of BRD7 gene. These findings will help to further understand and uncover the bio-functions of BRD7 gene involved in the pathogenesis of NPC.
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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.