ArticleThe Journal of biological chemistry2012
Intronic promoter drives the BORIS-regulated expression of FerT in colon carcinoma cells.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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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
8 citing papers in PubMed, 12 citations in OpenAlex.
- BORIS/CTCFL epigenetically reprograms clustered CTCF binding sites into alternative transcriptional start sites.Genome biology · 2024Article
- Fer and FerT: A New Regulatory Link between Sperm and Cancer Cells.International journal of molecular sciences · 2023Review
- The combined action of CTCF and its testis-specific paralog BORIS is essential for spermatogenesis.Nature communications · 2021Article
- Article
- BORIS: a key regulator of cancer stemness.Cancer cell international · 2018Review
- A novel Fer/FerT targeting compound selectively evokes metabolic stress and necrotic death in malignant cells.Nature communications · 2017Article
- BORIS, brother of the regulator of imprinted sites, is aberrantly expressed in hepatocellular carcinoma.Genetic testing and molecular biomarkers · 2013Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fer is an intracellular tyrosine kinase that accumulates in most mammalian tissues. A truncated variant of Fer, FerT, is uniquely detected in spermatogenic cells and is absent from normal somatic tissues. Here, we show that in addition to Fer, FerT also accumulates in CC cells and in metastases derived from colorectal tumors, but not in normal human cells. Thus, FerT is a new member of the CTA protein family. Transcription of the ferT gene in CC cells was found to be driven by an intronic promoter residing in intron 10 of the fer gene and to be regulated by another CTA, the Brother of the Regulator of Imprinted Sites (BORIS) transcription factor. BORIS binds to the ferT promoter and down-regulation of BORIS significantly decreases the expression of ferT in CC cells. Accumulation of the ferT RNA was also regulated by the DNA methylation status and paralleled the expression profile of the boris transcript. Accordingly, the intronic ferT promoter was found to be hypomethylated in cancer cells expressing the FerT protein, by comparison with non-expressers. Collectively, we show here that FerT is a new CTA whose accumulation in CC cells, commonly considered low CTA expressers, is controlled by a novel transcription regulatory mechanism.
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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.