Evidence map›Paper›PMID 20157762›Full record

ArticleJournal of neuro-oncology2010

HGF upregulates CXCR4 expression in gliomas via NF-kappaB: implications for glioma cell migration.

Mine Esencay, Elizabeth W Newcomb, David Zagzag

Open access · greenAbstract read
In one paragraph

Article in Journal of neuro-oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.6field-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

38 citing papers in PubMed, 61 citations in OpenAlex.

  1. Understanding the role of TNFR2 signaling in the tumor microenvironment of breast cancer.Journal of experimental & clinical cancer research : CR · 2024
    Review
  2. Review
  3. Review
  4. Immune response in glioma's microenvironment.Innovative surgical sciences · 2020
    Review
  5. Article
  6. Review
  7. Article
  8. MET in glioma: signaling pathways and targeted therapies.Journal of experimental & clinical cancer research : CR · 2019
    Review
  9. Article
  10. Targeting CXCL12/CXCR4 Axis in Tumor Immunotherapy.Current medicinal chemistry · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Oncogenic roles and drug target of CXCR4/CXCL12 axis in lung cancer and cancer stem cell.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  20. 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

3 authors at 1 institution in 1 country.

Mine EsencayMicrovascular and Molecular Neuro-Oncology Laboratory, New York University School of Medicine, New York, NY 10016, USA.
Elizabeth W Newcomb
David Zagzag
New York University · US

Funding

Invasion and Angiogenesis in Malignant GliomasR01CA100426 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ZAGZAG, DAVID · 2004 to 2008
$1.4M
NCI NIH HHS R01 CA100426
6 · The paper itself

Abstract

Invasion is a hallmark of malignant gliomas and is the main reason for therapeutic failure and recurrence of the tumor. CXCR4 is a key chemokine receptor implicated in glioma cell migration whose expression is regulated by hypoxia. Here, we report that hepatocyte growth factor (HGF) upregulated CXCR4 protein expression in glioma cells. HGF pre-treatment increased migration of U87MG and LN229 glioma cells towards the CXCR4 ligand, stromal cell-derived factor-1alpha (SDF-1alpha). AMD3100, a CXCR4 inhibitor, inhibited the increased migration of HGF pre-treated LN229 glioma cells towards SDF-1alpha. Following exposure to HGF and hypoxia, both cell lines showed nuclear translocation of NF-kappaB (p65). The HGF- and hypoxia-induced nuclear translocation of NF-kappaB (p65) involved phosphorylation and degradation of IkappaB-alpha. Knock-down of NF-kappaB expression inhibited the induction of CXCR4 expression in response to HGF, but not to hypoxia. However, knock-down of NF-kappaB expression inhibited the induction of CXCR4 expression in response to hypoxia in the presence of HGF. NF-kappaB mediated migration towards SDF-1alpha in response to HGF. Knock-down of NF-kappaB expression resulted in decreased migration of HGF pre-treated glioma cells towards SDF-1alpha. Therefore, HGF upregulates CXCR4 expression via NF-kappaB and leads to enhanced migration. To our knowledge, this is the first report to show that a crosstalk mediated by NF-kappaB exists between the SDF-1alpha/CXCR4 and HGF/c-Met axes relevant to glioma cell migration. These findings imply that effective inhibition of glioma invasion should be directed against several ligand/receptor signaling pathways.

Indexed as

BenzylaminesCell HypoxiaCell Line, TumorCell MovementChemokine CXCL12CyclamsDrug InteractionsGene Expression Regulation, NeoplasticGliomaHeterocyclic CompoundsHumansNerve Growth FactorNF-kappa BReceptors, CXCR4RNA, Small InterferingTime FactorsBenzylaminesChemokine CXCL12CXCR4 protein, humanCyclamsHeterocyclic CompoundsNerve Growth FactorNF-kappa BplerixaforReceptors, CXCR4RNA, Small Interfering

Identifiers

PMID20157762
PMCPMC3767998
OpenAlexW1978429383

What OpenQuestion holds

Textmetadata
LicenceTDM
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.