Evidence map›Paper›PMID 23865743›Full record

ArticleBMC cancer2013

CXCR7 is induced by hypoxia and mediates glioma cell migration towards SDF-1α.

Mine Esencay, Yasmeen Sarfraz, David Zagzag

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2013. 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, 53 citations in OpenAlex.

  1. Article
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  8. Crosstalk between CXCR4/ACKR3 and EGFR Signaling in Breast Cancer Cells.International journal of molecular sciences · 2022
    Article
  9. Review
  10. Article
  11. Review
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  13. Review
  14. Article
  15. Cancers · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. The unique structural and functional features of CXCL12.Cellular & molecular immunology · 2018
    Review
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

3 authors at 1 institution in 1 country.

Mine EsencayMicrovascular and Molecular Neuro-oncology Laboratory, New York University Langone Medical Center, New York, NY, USA.
Yasmeen Sarfraz
David Zagzag
NYU Langone Health · US

Funding

Intranasal Drug Delivery to Inhibit Glioma Angiogenesis and InvasionR21NS065380 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ZAGZAG, DAVID · 2009 to 2010
$482k
NINDS NIH HHS R21 NS065380
6 · The paper itself

Abstract

backgroundGlioblastomas, the most common and malignant brain tumors of the central nervous system, exhibit high invasive capacity, which hinders effective therapy. Therefore, intense efforts aimed at improved therapeutics are ongoing to delineate the molecular mechanisms governing glioma cell migration and invasion.

methodsIn order to perform the studies, we employed optimal cell culture methods and hypoxic conditions, lentivirus-mediated knockdown of protein expression, Western Blot analysis, migration assays and immunoprecipitation. We determined statistical significance by unpaired t-test.

resultsIn this report, we show that U87MG, LN229 and LN308 glioma cells express CXCR7 and that exposure to hypoxia upregulates CXCR7 protein expression in these cell lines. CXCR7-expressing U87MG, LN229 and LN308 glioma cells migrated towards stromal-derived factor (SDF)-1α/CXCL12 in hypoxic conditions in the Boyden chamber assays. While shRNA-mediated knockdown of CXCR7 expression did not affect the migration of any of the three cell lines in normoxic conditions, we observed a reduction in the migration of LN229 and LN308, but not U87MG, glioma cells towards SDF-1α in hypoxic conditions. In addition, knockdown of CXCR7 expression in LN229 and LN308 glioma cells decreased levels of SDF-1α-induced phosphorylation of ERK1/2 and Akt. Inhibiting CXCR4 in LN229 and LN308 glioma cells that were knocked down for CXCR7 did not further reduce migration towards SDF-1α in hypoxic conditions and did not affect the levels of phosphorylated ERK1/2 and Akt. Analysis of immunoprecipitated CXCR4 from LN229 and LN308 glioma cells revealed co-precipitated CXCR7.

conclusionsTaken together, our findings indicate that both CXCR4 and CXCR7 mediate glioma cell migration towards SDF-1α in hypoxic conditions and support the development of therapeutic agents targeting these receptors.

Indexed as

Cell MovementBlotting, WesternCell HypoxiaCell Line, TumorChemokine CXCL12Gene Knockdown TechniquesGliomaHumansImmunoprecipitationNeoplasm InvasivenessReceptors, CXCRReceptors, CXCR4ACKR3 protein, humanChemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanReceptors, CXCRReceptors, CXCR4

Identifiers

PMID23865743
PMCPMC3728118
OpenAlexW2049102551

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.