Evidence map›Paper›PMID 23258844›Full record

ArticleNeuro-oncology2013

Wnt/β-catenin signaling is a key downstream mediator of MET signaling in glioblastoma stem cells.

Kang Ho Kim, Ho Jun Seol, Eun Hee Kim, Jinguen Rheey, Hyun Jin Jin, Yeri Lee, Kyeung Min Joo, Jeongwu Lee, Do-Hyun Nam

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

80 citing papers in PubMed, 121 citations in OpenAlex.

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  18. Signaling pathways in brain tumors and therapeutic interventions.Signal transduction and targeted therapy · 2023
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20 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Kang Ho KimDepartment of Neurosurgery, Samsung Biomedical Research Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Gangnam-gu, Seoul 135-710, South Korea.
Ho Jun Seol
Eun Hee Kim
Jinguen Rheey
Hyun Jin Jin
Yeri Lee
Kyeung Min Joo
Jeongwu Lee
Do-Hyun Nam
Samsung Medical Center · KRSungkyunkwan University · KRSamsung (South Korea) · KRCleveland Clinic Lerner College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlioblastoma (GBM) is the most lethal and common type of primary brain tumor. Recent evidence suggests that a subpopulation of GBM cells (glioblastoma stem cells [GSCs]) is critical for tumor progression, invasion, and therapeutic resistance. We and others have demonstrated that MET, a receptor tyrosine kinase, positively regulates the stemness phenotype and radioresistance of GSCs. Here, we interrogated the downstream effector pathways of MET signaling in GSCs.

methodsWe have established a series of GSCs and xenograft tumors derived from freshly dissociated specimens from patients with GBM and characterized a subpopulation enriched with MET activation (MET(high/+)). Through global expression profiling and subsequent pathways analysis, we identified signaling pathways that are enriched in MET(high/+) populations, one of which is Wnt/β-catenin signaling pathway. To determine molecular interaction and the biological consequences of MET and Wnt/β-catenin signaling, we used pharmacological and shRNA-mediated genetic inhibition and performed various molecular and cellular analyses, including flow cytometry, immunohistochemistry, and clonogenicity assays.

resultsWe found that Wnt/β-catenin signaling is highly active in MET(high/+) cells, compared with bulk tumor cells. We also showed that Wnt/β-catenin signaling activities in GBM are directly modulated by the addition of ligand-mediated MET activation or MET inhibition. Furthermore, the ectopic expression of active-β-catenin (S37A and S45Y) rescued the phenotypic effects caused by MET inhibition.

conclusionThese data suggest that Wnt/β-catenin signaling is a key downstream effector of MET signaling and contributes to the maintenance of GSC and GBM malignancy.

Indexed as

Wnt Signaling PathwayAnimalsApoptosisBiomarkers, TumorBlotting, WesternBrain NeoplasmsCell ProliferationGene Expression ProfilingGlioblastomaHumansImmunoenzyme TechniquesLuciferasesMiceMice, NudeNeoplastic Stem CellsOligonucleotide Array Sequence AnalysisBiomarkers, TumorLuciferasesMET protein, humanProto-Oncogene Proteins c-metRNA, Messenger

Identifiers

PMID23258844
PMCPMC3548587
OpenAlexW2119092375

What OpenQuestion holds

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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.