Evidence map›Paper›PMID 18507857›Full record

ArticleMolecular cancer2008

Altered splicing of CEACAM1 in breast cancer: identification of regulatory sequences that control splicing of CEACAM1 into long or short cytoplasmic domain isoforms.

Shikha Gaur, John E Shively, Yun Yen, Rajesh K Gaur

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Structural aspects of CEACAM1 interactions.European journal of clinical investigation · 2024
    Review
  4. CEACAM1 in vascular homeostasis and inflammation.European journal of clinical investigation · 2024
    Review
  5. Review
  6. Article
  7. Review
  8. CEACAM expression in anFrontiers in immunology · 2023
    Article
  9. Targeting alternative splicing in cancer immunotherapy.Frontiers in cell and developmental biology · 2023
    Review
  10. Article
  11. Frontiers in genetics · 2021
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. 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

4 authors at 2 institutions in 1 country.

Shikha GaurDivision of Molecular Biology, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA. sgaur@coh.org
John E Shively
Yun Yen
Rajesh K Gaur
Beckman Research InstituteCity of Hope · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCarcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), a cell adhesion molecule expressed in a variety of cell types is a putative tumor suppressor gene. Alternative splicing of CEACAM1 generates 11 different splice variants, which include 1-4 ectodomains with either short or long cytoplasmic domain generated by the exclusion (CEACAM1-S) or inclusion (CEACAM1-L) of exon 7. Studies in rodents indicate that optimal ratios of CEACAM1 splice variants are required to inhibit colonic tumor cell growth.

resultsWe show that CEACAM1 is expressed in a tissue specific manner with significant differences in the ratios of its short (CEACAM1-S) and long (CEACAM1-L) cytoplasmic domain splice variants. Importantly, we find dramatic differences between the ratios of S:L isoforms in normal breast tissues versus breast cancer specimens, suggesting that altered splicing of CEACAM1 may play an important role in tumorogenesis. Furthermore, we have identified two regulatory cis-acting elements required for the alternative splicing of CEACAM1. Replacement of these regulatory elements by human beta-globin exon sequences resulted in exon 7-skipped mRNA as the predominant product. Interestingly, while insertion of exon 7 in a beta-globin reporter gene resulted in its skipping, exon 7 along with the flanking intron sequences recapitulated the alternative splicing of CEACAM1.

conclusionOur results indicate that a network of regulatory elements control the alternative splicing of CEACAM1. These findings may have important implications in therapeutic modalities of CEACAM1 linked human diseases.

Indexed as

Alternative SplicingAntigens, CDBreast NeoplasmsCell Adhesion MoleculesCell Line, TumorCytoplasmExonsGene Expression Regulation, NeoplasticHealthHumansIntronsProtein IsoformsRegulatory Sequences, Nucleic AcidAntigens, CDCD66 antigensCell Adhesion MoleculesProtein Isoforms

Identifiers

PMID18507857
PMCPMC2490704
OpenAlexW2099503871

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.