ArticleCancer immunity2013
BORIS/CTCFL mRNA isoform expression and epigenetic regulation in epithelial ovarian cancer.
Article in Cancer immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Role of DNA methylation and non‑coding RNAs expression in pathogenesis, detection, prognosis, and therapy‑resistant ovarian carcinoma (Review).Molecular medicine reports · 2025Review
- The potential value of cancer-testis antigens in ovarian cancer: Prognostic markers and targets for immunotherapy.Immunity, inflammation and disease · 2024Review
- The exon 12-containing LHX6 isoforms promote cervical cancer cell proliferation by regulating the MAPK signaling pathway.Cancer medicine · 2022Article
- Molecular Regulation of Androgen Receptors in Major Female Reproductive System Cancers.International journal of molecular sciences · 2022Review
- Nucleic acid vaccination strategies for ovarian cancer.Frontiers in bioengineering and biotechnology · 2022Review
- 3D chromatin architecture and epigenetic regulation in cancer stem cells.Protein & cell · 2021Review
- Ovarian Cancer: Therapeutic Strategies to Overcome Immune Suppression.Advances in experimental medicine and biology · 2021Article
- Revisiting 3D chromatin architecture in cancer development and progression.Nucleic acids research · 2020Review
- Genome-wide bioinformatics analysis reveals CTCFL is upregulated in high-grade epithelial ovarian cancer.Oncology letters · 2019Article
- The epigenetic factor BORIS (CTCFL) controls the androgen receptor regulatory network in ovarian cancer.Oncogenesis · 2019Article
- Epigenetic activation of POTE genes in ovarian cancer.Epigenetics · 2019Article
- Cancer-testis antigens in ovarian cancer: implication for biomarkers and therapeutic targets.Journal of ovarian research · 2019Review
- Targeting CTCFL/BORIS for the immunotherapy of cancer.Cancer immunology, immunotherapy : CII · 2018Review
- BORIS: a key regulator of cancer stemness.Cancer cell international · 2018Review
- Intragenic DNA methylation and BORIS-mediated cancer-specific splicing contribute to the Warburg effect.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Brother of the regulator of the imprinted site (BORIS) variant subfamily 6 is involved in cervical cancer stemness and can be a target of immunotherapy.Oncotarget · 2016Article
- Expression of the CTCFL Gene during Mouse Embryogenesis Causes Growth Retardation, Postnatal Lethality, and Dysregulation of the Transforming Growth Factor β Pathway.Molecular and cellular biology · 2015Article
- CTCFL (BORIS) mRNA Expression in a Peripheral Giant Cell Granuloma of the Oral Cavity.Case reports in dentistry · 2014Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cancer germline (CG) genes are normally expressed in germ cells and aberrantly expressed in a variety of cancers; their immunogenicity has led to the widespread development of cancer vaccines targeting these antigens. BORIS/CTCFL is an autosomal CG antigen and promising cancer vaccine target. BORIS is the only known paralog of CTCF, a gene intimately involved in genomic imprinting, chromatin insulation, and nuclear regulation. We have previously shown that BORIS is expressed in epithelial ovarian cancer (EOC) and that its expression coincides with promoter and global DNA hypomethylation. Recently, 23 different BORIS mRNA variants have been described, and have been functionally grouped into six BORIS isoform families (sf1-sf6). In the present study, we have characterized the expression of BORIS isoform families in normal ovary (NO) and EOC, the latter of which were selected to include two groups with widely varying global DNA methylation status. We find selective expression of BORIS isoform families in NO, which becomes altered in EOC, primarily by the activation of BORIS sf1 in EOC. When comparing EOC samples based on methylation status, we find that BORIS sf1 and sf2 isoform families are selectively activated in globally hypomethylated tumors. In contrast, CTCF is downregulated in EOC, and the ratio of BORIS sf1, sf2, and sf6 isoform families as a function of CTCF is elevated in hypomethylated tumors. Finally, the expression of all BORIS isoform families was induced to varying extents by epigenetic modulatory drugs in EOC cell lines, particularly when DNMT and HDAC inhibitors were used in combination.
Indexed as
Identifiers
23390377PMC3559194W2122911471What 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.