Evidence map›Paper›PMID 24650050›Full record

ArticleMolecular cancer2014

IRF-1 regulates alternative mRNA splicing of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) in breast epithelial cells generating an immunoreceptor tyrosine-based inhibition motif (ITIM) containing isoform.

Kenneth J Dery, Maciej Kujawski, David Grunert, Xiwei Wu, Tung Ngyuen, Celeste Cheung, John H Yim, John E Shively

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.6field-weighted citation impact, top 32% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Mechanism and function of CEACAM1 splice isoforms.European journal of clinical investigation · 2024
    Review
  5. Regulation of lipid storage and inflammation in the liver by CEACAM1.European journal of clinical investigation · 2024
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. CEACAM expression in anFrontiers in immunology · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Kenneth J Dery
Maciej Kujawski
David Grunert
Xiwei Wu
Tung Ngyuen
Celeste Cheung
John H Yim
John E ShivelyDepartments of Immunology, Beckman Research Institute, City of Hope, Duarte, California, USA. jshively@coh.org.
City Of Hope National Medical Center · USBeckman Research InstituteCity of Hope · US

Funding

Transgenic Mouse FacilityP30CA033572 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI XIWEI WU · 1985 to 2026
$86.3M
NCI NIH HHS P30 CA033572
6 · The paper itself

Abstract

backgroundInterferon regulatory factor-1 (IRF-1) is a master regulator of IFN-γ induced gene transcription. Previously we have shown that IRF-1 transcriptionally induces CEACAM1 via an ISRE (Interferon-Stimulated Response Element) in its promoter. CEACAM1 pre-mRNA undergoes extensive alternative splicing (AS) generating isoforms to produce either a short (S) cytoplasmic domain expressed primarily in epithelial cells or as an ITIM-containing long (L) isoform in immune cells.

methodsThe transcriptional and molecular mechanism of CEACAM1 minigenes AS containing promoter ISREs mutations in the breast epithelial, MDA-MB-468, cell line was detected using flow cytometry. In addition, transcriptome sequencing was utilized to determine whether IRF-1 could direct the AS of other genes as well. Tumor xenografts were used to evaluate CEACAM1 isoform expression on the leading edge of breast tumor cells.

resultsIn the present study, we provide evidence that CEACAM1's promoter and variable exon 7 cross-talk allowing IRF-1 to direct AS events. Transcriptome sequencing shows that IRF-1 can also induce the global AS of genes involved in regulation of growth and differentiation as well as genes of the cytokine family. Furthermore, MDA-MB-468 cells grown as tumor xenografts exhibit an AS switch to the L-isoform of CEACAM1, demonstrating that an in vivo inflammatory milieu is also capable of generating the AS switch, similar to that found in human breast cancers Mol Cancer 7:46, 2008.

conclusionsThe novel AS regulatory activities attributed to IRF-1 indicate that the IFN-γ response involves a global change in both gene transcription and AS in breast epithelial cells.

Indexed as

Alternative SplicingAnimalsAntigens, CDBreastCell Adhesion MoleculesCell Line, TumorEpithelial CellsFemaleGene Expression Regulation, NeoplasticHumansImmunoreceptor Tyrosine-Based Inhibition MotifInterferon-gammaInterferon Regulatory Factor-1MiceProtein IsoformsXenograft Model Antitumor AssaysAntigens, CDCD66 antigensCell Adhesion MoleculesInterferon-gammaInterferon Regulatory Factor-1Protein Isoforms

Identifiers

PMID24650050
PMCPMC4113144
OpenAlexW2096631439

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.