Evidence map›Paper›PMID 27527869›Full record

ArticleOncotarget2017

Epithelial membrane protein 3 regulates TGF-β signaling activation in CD44-high glioblastoma.

Fu Jun, Jidong Hong, Qin Liu, Yong Guo, Yiwei Liao, Jianghai Huang, Sailan Wen, Liangfang Shen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.8field-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

36 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  3. Investigation ofBiology · 2024
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  6. EMP3: A promising biomarker for tumor prognosis and targeted cancer therapy.Cancer biomarkers : section A of Disease markers · 2024
    Review
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  14. Review
  15. EMP3 mediates glioblastoma-associated macrophage infiltration to drive T cell exclusion.Journal of experimental & clinical cancer research : CR · 2021
    Article
  16. Article
  17. Article
  18. Observational
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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 2 institutions in 1 country.

Fu JunDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, P. R China.
Jidong HongDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, P. R China.
Qin LiuDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, P. R China.
Yong GuoDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, P. R China.
Yiwei LiaoDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, P. R China.
Jianghai HuangDepartment of Pathology, The Second Xiangya Hospital, Central South University, Changsha, P. R China.
Sailan WenDepartment of Pathology, The Second Xiangya Hospital, Central South University, Changsha, P. R China.
Liangfang ShenDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, P. R China.
Central South University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although epithelial membrane protein 3 (EMP3) has been implicated as a candidate tumor suppressor gene for low grade glioma, its biological function in glioblastoma multiforme (GBM) still remains poorly understood. Herein, we showed that EMP3 was highly expressed in CD44-high primary GBMs. Depletion of EMP3 expression suppressed cell proliferation, impaired in vitro tumorigenic potential and induced apoptosis in CD44-high GBM cell lines. We also identified TGF-β/Smad2/3 signaling pathway as a potential target of EMP3. EMP3 interacts with TGF-β receptor type 2 (TGFBR2) upon TGF-β stimulation in GBM cells. Consequently, the EMP3-TGFBR2 interaction regulates TGF-β/Smad2/3 signaling activation and positively impacts on TGF-β-stimulated gene expression and cell proliferation in vitro and in vivo. Highly correlated protein expression of EMP3 and TGF-β/Smad2/3 signaling pathway components was also observed in GBM specimens, confirming the clinical relevancy of activated EMP3/TGF-β/Smad2/3 signaling in GBM. In conclusion, our findings revealed that EMP3 might be a potential target for CD44-high GBMs and highlight the essential functions of EMP3 in TGF-β/Smad2/3 signaling activation and tumor progression.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorBrain NeoplasmsCell ProliferationGlioblastomaHumansHyaluronan ReceptorsMembrane GlycoproteinsMiceMice, NudeNeoplasm GradingPrognosisSignal TransductionSmad2 ProteinBiomarkers, TumorCD44 protein, humanEMP3 protein, humanHyaluronan ReceptorsMembrane GlycoproteinsSmad2 ProteinSMAD2 protein, humanTransforming Growth Factor betaEMP3gliblastomaTGFBR2TGF-βtumorigenesis

Identifiers

PMID27527869
PMCPMC5362410
OpenAlexW2494703521

What OpenQuestion holds

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Registered trials

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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.