Evidence map›Paper›PMID 24699049›Full record

ArticlePloS one2014

SDA, a DNA aptamer inhibiting E- and P-selectin mediated adhesion of cancer and leukemia cells, the first and pivotal step in transendothelial migration during metastasis formation.

Rassa Faryammanesh, Tobias Lange, Eileen Magbanua, Sina Haas, Cindy Meyer, Daniel Wicklein, Udo Schumacher, Ulrich Hahn

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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  5. Review
  6. Article
  7. [Research advances in the role of aptamers in the diagnosis and targeted therapy of pediatric cancer].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Arresting the colonial destiny of metastatic seeds with DNA aptamers.Molecular therapy : the journal of the American Society of Gene Therapy · 2015
    Article
  13. 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.

Rassa FaryammaneshHamburg University, MIN-Faculty, Chemistry Department, Institute for Biochemistry and Molecular Biology, Hamburg, Germany.
Tobias LangeUniversity Medical Center Hamburg-Eppendorf, University Cancer Center, Institute of Anatomy and Experimental Morphology, Hamburg, Germany.
Eileen MagbanuaHamburg University, MIN-Faculty, Chemistry Department, Institute for Biochemistry and Molecular Biology, Hamburg, Germany.
Sina HaasHamburg University, MIN-Faculty, Chemistry Department, Institute for Biochemistry and Molecular Biology, Hamburg, Germany.
Cindy MeyerHamburg University, MIN-Faculty, Chemistry Department, Institute for Biochemistry and Molecular Biology, Hamburg, Germany.
Daniel WickleinUniversity Medical Center Hamburg-Eppendorf, University Cancer Center, Institute of Anatomy and Experimental Morphology, Hamburg, Germany.
Udo SchumacherUniversity Medical Center Hamburg-Eppendorf, University Cancer Center, Institute of Anatomy and Experimental Morphology, Hamburg, Germany.
Ulrich HahnHamburg University, MIN-Faculty, Chemistry Department, Institute for Biochemistry and Molecular Biology, Hamburg, Germany.
Universität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DEUniversity Cancer Center Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial (E-) and platelet (P-) selectin mediated adhesion of tumor cells to vascular endothelium is a pivotal step of hematogenous metastasis formation. Recent studies have demonstrated that selectin deficiency significantly reduces metastasis formation in vivo. We selected an E- and P-Selectin specific DNA Aptamer (SDA) via SELEX (Systematic Evolution of Ligands by EXponential enrichment) with a K(d) value of approximately 100 nM and the capability of inhibiting the interaction between selectin and its ligands. Employing human colorectal cancer (HT29) and leukemia (EOL-1) cell lines we could demonstrate an anti-adhesive effect for SDA in vitro. Under physiological shear stress conditions in a laminar flow adhesion assay, SDA inhibited dynamic tumor cell adhesion to immobilized E- or P-selectin. The stability of SDA for more than two hours allowed its application in cell-cell adhesion assays in cell culture medium. When adhesion of HT29 cells to TNFα-stimulated E-selectin presenting human pulmonary microvascular endothelial cells was analyzed, inhibition via SDA could be demonstrated as well. In conclusion, SDA is a potential new therapeutic agent that antagonizes selectin-mediated adhesion during metastasis formation in human malignancies.

Indexed as

Aptamers, NucleotideCell AdhesionCell ProliferationCells, CulturedColorectal NeoplasmsEndothelium, VascularE-SelectinHumansLeukemiaLungP-SelectinSELEX Aptamer TechniqueTransendothelial and Transepithelial MigrationAptamers, NucleotideE-SelectinP-Selectin

Identifiers

PMID24699049
PMCPMC3974700
OpenAlexW1976481739

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.