Evidence map›Paper›PMID 31233190›Full record

ArticleOncology reports2019

Epithelial membrane protein 1 promotes glioblastoma progression through the PI3K/AKT/mTOR signaling pathway.

Lifeng Miao, Zheng Jiang, Jiwei Wang, Ning Yang, Qichao Qi, Wenjing Zhou, Zichao Feng, Wenjie Li, Qing Zhang, Bin Huang and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.6field-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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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  20. Prognostic Relevance of Expression ofFrontiers in oncology · 2021
    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

14 authors at 1 institution in 1 country.

Lifeng MiaoDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Zheng JiangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Jiwei WangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Ning YangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Qichao QiDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Wenjing ZhouDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Zichao FengDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Wenjie LiDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Qing ZhangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Bin HuangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Anjing ChenDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Di ZhangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Peng ZhaoDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Xingang LiDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Key Laboratory of Brain Functional Remodeling, Jinan, Shandong 250012, P.R. China.
Qilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most malignant intracranial tumor. Although the affected patients are usually treated with surgery combined with radiotherapy and chemotherapy, the median survival time for GBM patients is still approximately 12‑14 months. Identifying the key molecular mechanisms and targets of GBM development may therefore lead to the development of improved therapies for GBM patients. In the present study, the clinical significance and potential function of epithelial membrane protein 1 (EMP1) in malignant gliomas were investigated. Increased EMP1 expression was associated with increasing tumor grade (P<0.001) and worse prognosis in patients (P<0.001) based on TCGA, Rembrandt and CGGA databases for human gliomas. In vitro, gene silencing of EMP1 in U87MG and P3 GBM (primary glioma) cells significantly inhibited tumor proliferation and invasion. In addition, it was revealed that activation of the PI3K/AKT/mTOR signaling pathway is the driving force of EMP1‑promoted glioma progression. Finally, it was demonstrated, using an intracranial GBM animal model, that EMP1 knockdown significantly inhibits tumor growth in vivo and increases overall survival in tumor‑bearing animals. Our research provides new insights into the molecular mechanisms underlying EMP1 knockdown‑mediated inhibition of GBM cell invasion and raises the possibility that targeting of EMP1 may represent a promising strategy for the treatment of GBM.

Indexed as

AnimalsApoptosisBiomarkers, TumorBrain NeoplasmsCase-Control StudiesCell ProliferationDisease ProgressionFollow-Up StudiesGene Expression Regulation, NeoplasticGlioblastomaHumansMaleMiceMice, NudeNeoplasm ProteinsPhosphatidylinositol 3-KinasesBiomarkers, Tumorepithelial membrane protein-1MTOR protein, humanNeoplasm ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Cell SurfaceTOR Serine-Threonine Kinases

Identifiers

PMID31233190
PMCPMC6609345
OpenAlexW2951337951

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.