Evidence map›Paper›PMID 26119933›Full record

ArticleOncogene2016

Glioma invasion mediated by the p75 neurotrophin receptor (p75(NTR)/CD271) requires regulated interaction with PDLIM1.

B Y Ahn, R F G Saldanha-Gama, J J Rahn, X Hao, J Zhang, N-H Dang, M Alshehri, S M Robbins, D L Senger

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 19% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Nerve growth factor receptor (NGFR): A key player in glioblastoma progression.Biochimica et biophysica acta. Reviews on cancer · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Exploring the PDZ, DUF, and LIM Domains of Pdlim5 in Dendrite Branching.International journal of molecular sciences · 2024
    Article
  14. Gene Expression Patterns Associated with Survival in Glioblastoma.International journal of molecular sciences · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  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

9 authors at 1 institution in 1 country.

B Y AhnSouthern Alberta Cancer Research Institute, University of Calgary, Calgary, Alberta, Canada.
R F G Saldanha-GamaSouthern Alberta Cancer Research Institute, University of Calgary, Calgary, Alberta, Canada.
J J RahnSouthern Alberta Cancer Research Institute, University of Calgary, Calgary, Alberta, Canada.
X HaoSouthern Alberta Cancer Research Institute, University of Calgary, Calgary, Alberta, Canada.
J ZhangSouthern Alberta Cancer Research Institute, University of Calgary, Calgary, Alberta, Canada.
N-H DangSouthern Alberta Cancer Research Institute, University of Calgary, Calgary, Alberta, Canada.
M AlshehriSouthern Alberta Cancer Research Institute, University of Calgary, Calgary, Alberta, Canada.
S M RobbinsSouthern Alberta Cancer Research Institute, University of Calgary, Calgary, Alberta, Canada.
D L SengerSouthern Alberta Cancer Research Institute, University of Calgary, Calgary, Alberta, Canada.
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The invasive nature of glioblastoma renders them incurable by current therapeutic interventions. Using a novel invasive human glioma model, we previously identified the neurotrophin receptor p75(NTR) (aka CD271) as a mediator of glioma invasion. Herein, we provide evidence that preventing phosphorylation of p75(NTR) on S303 by pharmacological inhibition of PKA, or by a mutational strategy (S303G), cripples p75(NTR)-mediated glioma invasion resulting in serine phosphorylation within the C-terminal PDZ-binding motif (SPV) of p75(NTR). Consistent with this, deletion (ΔSPV) or mutation (SPM) of the PDZ motif results in abrogation of p75(NTR)-mediated invasion. Using a peptide-based strategy, we identified PDLIM1 as a novel signaling adaptor for p75(NTR) and provide the first evidence for a regulated interaction via S425 phosphorylation. Importantly, PDLIM1 was shown to interact with p75(NTR) in highly invasive patient-derived glioma stem cells/tumor-initiating cells and shRNA knockdown of PDLIM1 in vitro and in vivo results in complete ablation of p75(NTR)-mediated invasion. Collectively, these data demonstrate a requirement for a regulated interaction of p75(NTR) with PDLIM1 and suggest that targeting either the PDZ domain interactions and/or the phosphorylation of p75(NTR) by PKA could provide therapeutic strategies for patients with glioblastoma.

Indexed as

AnimalsBrain NeoplasmsCell Line, TumorCyclic AMP-Dependent Protein KinasesFemaleGlioblastomaHumansLIM Domain ProteinsMiceMice, SCIDNeoplasm InvasivenessNerve Tissue ProteinsPDZ DomainsPhosphorylationReceptors, Nerve Growth FactorRNA InterferenceCyclic AMP-Dependent Protein KinasesLDB2 protein, humanLIM Domain ProteinsNerve Tissue ProteinsNGFR protein, humanReceptors, Nerve Growth FactorRNA, Small InterferingTranscription Factors

Identifiers

PMID26119933
PMCPMC4800290
OpenAlexW1534083990

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.