Evidence map›Paper›PMID 23021083›Full record

ArticleMolecular cancer2012

Focal overexpression of CEACAM6 contributes to enhanced tumourigenesis in head and neck cancer via suppression of apoptosis.

Sarina Cameron, Lilia Merida de Long, Mehlika Hazar-Rethinam, Eleni Topkas, Liliana Endo-Munoz, Andrew Cumming, Orla Gannon, Alexander Guminski, Nicholas Saunders

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. The emerging roles of CEACAM6 in human cancer (Review).International journal of oncology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Efficacy of bivalentHeliyon · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Integrated Analysis RevealsFrontiers in oncology · 2020
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  13. Article
  14. Article
  15. Downregulation ofAmerican journal of cancer research · 2018
    Article
  16. Article
  17. Article
  18. Expression of Carcinoembryonic Cell Adhesion Molecule 6 and Alveolar Epithelial Cell Markers in Lungs of Human Infants with Chronic Lung Disease.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2015
    Article
  19. 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

9 authors at 2 institutions in 1 country.

Sarina CameronUniversity of Queensland Diamantina Institute, Epithelial Pathobiology Group, Princess Alexandra Hospital, Queensland, Australia.
Lilia Merida de Long
Mehlika Hazar-Rethinam
Eleni Topkas
Liliana Endo-Munoz
Andrew Cumming
Orla Gannon
Alexander Guminski
Nicholas Saunders
Princess Alexandra Hospital · AUThe University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOverexpression of CEACAM6 has been reported for a number of malignancies. However, the mechanism of how CEACAM6 contributes to cancer formation and its role in head and neck squamous cell carcinoma (HNSCC) remains unclear. Therefore, we examined the role of CEACAM6 in head and neck squamous cell carcinoma (HNSCC).

methodsCEACAM6 expression was examined in normal squamous epithelia as well as a number of patient HNSCC samples and tumours derived from HNSCC cell lines injected into NOD/SCID mice. CEACAM6 expression was manipulated in HNSCC cell lines by shRNA-mediated CEACAM6 knockdown or virally-delivered overexpression of CEACAM6. The role of CEACAM6 in tumour growth and chemotherapeutic sensitivity was then assessed in vivo and in vitro respectively.

resultsCEACAM6 expression was significantly increased in highly tumourigenic HNSCC cell lines when compared to poorly tumourigenic HNSCC cell lines. Moreover, HNSCC patient tumours demonstrated focal expression of CEACAM6. Functional investigation of CEACAM6, involving over-expression and knock down studies, demonstrated that CEACAM6 over-expression could enhance tumour initiating activity and tumour growth via activation of AKT and suppression of caspase-3 mediated cell death.

conclusionWe report that CEACAM6 is focally overexpressed in a large fraction of human HNSCCs in situ. We also show that over-expression of CEACAM6 increases tumour growth and tumour initiating activity by suppressing PI3K/AKT-dependent apoptosis of HNSCC in a xenotransplant model of HNSCC. Finally, our studies indicate that foci of CEACAM6 expressing cells are selectively ablated by treatment of xenotransplant tumours with pharmacological inhibitors of PI3K/AKT in vivo.

Indexed as

Gene ExpressionAnimalsAntigens, CDApoptosisCarcinoma, Squamous CellCell Adhesion MoleculesCell Line, TumorCell ProliferationCell Transformation, NeoplasticGene Knockdown TechniquesGPI-Linked ProteinsHead and Neck NeoplasmsHumansImidazolesMiceMice, Inbred NOD8-(6-methoxypyridin-3-yl)-3-methyl-1-(4-piperazin-1-yl-3-trifluoromethylphenyl)-1,3-dihydroimidazo(4,5-c)quinolin-2-oneAntigens, CDCEACAM6 protein, humanCell Adhesion MoleculesGPI-Linked ProteinsImidazolesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktQuinolines

Identifiers

PMID23021083
PMCPMC3515475
OpenAlexW2170922257

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.