Evidence map›Paper›PMID 24586375›Full record

ArticlePloS one2014

DNA aptamers against exon v10 of CD44 inhibit breast cancer cell migration.

Joji Iida, Rebecca Clancy, Jesse Dorchak, Richard I Somiari, Stella Somiari, Mary Lou Cutler, Richard J Mural, Craig D Shriver

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  10. Review
  11. p63 inhibits CD44Experimental and therapeutic medicine · 2017
    Article
  12. Review
  13. Article
  14. Review
  15. Triple Negative Breast Cancer: Nanosolutions for a Big Challenge.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2015
    Article
  16. Article
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.

Joji IidaDepartment of Cell Biology, Windber Research Institute, Windber, Pennsylvania, United States of America.
Rebecca ClancyDepartment of Cell Biology, Windber Research Institute, Windber, Pennsylvania, United States of America.
Jesse DorchakDepartment of Cell Biology, Windber Research Institute, Windber, Pennsylvania, United States of America.
Richard I SomiariITSI-Biosciences, Johnstown, Pennsylvania, United States of America.
Stella SomiariDepartment of Cell Biology, Windber Research Institute, Windber, Pennsylvania, United States of America.
Mary Lou CutlerDepartment of Pathology, Uniformed Services University of the Health Science, Bethesda, Maryland, United States of America.
Richard J MuralWindber Research Institute, Windber, Pennsylvania, United States of America.
Craig D ShriverDepartment of Surgery, Walter-Reed Army Medical Center, Bethesda, Maryland, United States of America.
Windber Research Institute · USUniformed Services University of the Health Sciences · USWalter Reed Army Institute of Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD44 adhesion molecules are expressed in many breast cancer cells and have been demonstrated to play a key role in regulating malignant phenotypes such as growth, migration, and invasion. CD44 is an integral transmembrane protein encoded by a single 20-exon gene. The diversity of the biological functions of CD44 is the result of the various splicing variants of these exons. Previous studies suggest that exon v10 of CD44 plays a key role in promoting cancer invasion and metastasis, however, the molecular mechanisms are not clear. Given the fact that exon v10 is in the ectodomain of CD44, we hypothesized that CD44 forms a molecular complex with other cell surface molecules through exon v10 in order to promote migration of breast cancer cells. In order to test this hypothesis, we selected DNA aptamers that specifically bound to CD44 exon v10 using Systematic Evolution of Ligands by Exponential Enrichment (SELEX). We selected aptamers that inhibited migration of breast cancer cells. Co-immunoprecipitation studies demonstrated that EphA2 was co-precipitated with CD44. Pull-down studies demonstrated that recombinant CD44 exon v10 bound to EphA2 and more importantly aptamers that inhibited migration also prevented the binding of EphA2 to exon v10. These results suggest that CD44 forms a molecular complex with EphA2 on the breast cancer cell surface and this complex plays a key role in enhancing breast cancer migration. These results provide insight not only for characterizing mechanisms of breast cancer migration but also for developing target-specific therapy for breast cancers and possibly other cancer types expressing CD44 exon v10.

Indexed as

Cell MovementExonsAptamers, NucleotideBase SequenceBreast NeoplasmsCell Line, TumorDisease ProgressionHumansHyaluronan ReceptorsPeptidesReceptor, EphA2SELEX Aptamer TechniqueSubstrate SpecificityAptamers, NucleotideHyaluronan ReceptorsPeptidesReceptor, EphA2

Identifiers

PMID24586375
PMCPMC3929491
OpenAlexW2087641315

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.