ArticleNucleic acids research2007
Expression of the CTCF-paralogous cancer-testis gene, brother of the regulator of imprinted sites (BORIS), is regulated by three alternative promoters modulated by CpG methylation and by CTCF and p53 transcription factors.
Article in Nucleic acids research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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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.
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Who cites it
55 citing papers in PubMed, 105 citations in OpenAlex.
- Unveiling the significance of cancer-testis antigens and their implications for immunotherapy in glioma.Discover oncology · 2024Review
- The potential value of cancer-testis antigens in ovarian cancer: Prognostic markers and targets for immunotherapy.Immunity, inflammation and disease · 2024Review
- Review
- Association of mutation and expression of the brother of the regulator of imprinted sites (BORIS) gene with breast cancer progression.Oncotarget · 2023Article
- Review
- Ectopic expression of meiotic cohesin generates chromosome instability in cancer cell line.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- BTApep-TAT peptide inhibits ADP-ribosylation of BORIS to induce DNA damage in cancer.Molecular cancer · 2022Article
- Kita-Kyushu Lung Cancer Antigen-1 (KK-LC-1): A Promising Cancer Testis Antigen.Aging and disease · 2022Review
- CTCFL regulates the PI3K-Akt pathway and it is a target for personalized ovarian cancer therapy.NPJ systems biology and applications · 2022Article
- Suprabasin: Role in human cancers and other diseases.Molecular biology reports · 2022Review
- Role and Clinical Utility of Cancer/Testis Antigens in Head and Neck Squamous Cell Carcinoma.Cancers · 2021Review
- The combined action of CTCF and its testis-specific paralog BORIS is essential for spermatogenesis.Nature communications · 2021Article
- Higher ETV5 Expression Associates With Poor 5-Florouracil-Based Adjuvant Therapy Response in Colon Cancer.Frontiers in pharmacology · 2020Article
- BORIS/CTCFL promotes a switch from a proliferative towards an invasive phenotype in melanoma cells.Cell death discovery · 2020Article
- Cancer-testis antigens in ovarian cancer: implication for biomarkers and therapeutic targets.Journal of ovarian research · 2019Review
- Article
- Immunogenomics Analysis Reveals that TP53 Mutations Inhibit Tumor Immunity in Gastric Cancer.Translational oncology · 2018Article
- A Comprehensive Immunologic Portrait of Triple-Negative Breast Cancer.Translational oncology · 2018Article
- Discovering a binary CTCF code with a little help from BORIS.Nucleus (Austin, Tex.) · 2018Review
- BORIS: a key regulator of cancer stemness.Cancer cell international · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
BORIS, like other members of the 'cancer/testis antigen' family, is normally expressed in testicular germ cells and repressed in somatic cells, but is aberrantly activated in cancers. To understand regulatory mechanisms governing human BORIS expression, we characterized its 5'-flanking region. Using 5' RACE, we identified three promoters, designated A, B and C, corresponding to transcription start sites at -1447, -899 and -658 bp upstream of the first ATG. Alternative promoter usage generated at least five alternatively spliced BORIS mRNAs with different half-lives determined by varying 5'-UTRs. In normal testis, BORIS is transcribed from all three promoters, but 84% of the 30 cancer cell lines tested used only promoter(s) A and/or C while the others utilized primarily promoters B and C. The differences in promoter usage between normal and cancer cells suggested that they were subject to differential regulation. We found that DNA methylation and functional p53 contributes to the negative regulation of each promoter. Moreover, reduction of CTCF in normally BORIS-negative human fibroblasts resulted in derepression of BORIS promoters. These results provide a mechanistic basis for understanding cancer-related associations between haploinsufficiency of CTCF and BORIS derepression, and between the lack of functional p53 and aberrant activation of BORIS.
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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.