Evidence map›Paper›PMID 33369441›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2020

Involvement of EGFR, ERK-1,2 and AKT-1,2 Activity on Human Glioma Cell Growth.

Amir Alahverdi, Ehsan Arefian, Masoud Soleimani, Jafar Ai, Aaliakbar Yousefi-Ahmadipour, Abouzar Babaei, Md Shahidul Islam, Somayeh Ebrahimi-Barough

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Current Research Trends in Glioblastoma: Focus on Receptor Tyrosine Kinases.International journal of molecular sciences · 2025
    Review
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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 3 institutions in 1 country.

Amir AlahverdiDepartment of Tissue Engineering and Applied Cell Sciences, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Ehsan ArefianDepartment of Microbiology, School of Biology, College of Science, University of Tehran, Tehran, Iran.
Masoud SoleimaniDepartment of Hematology, Faculty of Medical Science, Tarbiat Modares University, Tehran, Iran.ORCID 0000-0003-1972-7771
Jafar AiDepartment of Tissue Engineering and Applied Cell Sciences, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Aaliakbar Yousefi-AhmadipourDepartment of Laboratory Sciences, School of Allied Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Abouzar BabaeiDepartment of Virology, Faculty of Medical Science, Tarbiat Modares University, Tehran, Iran.
Md Shahidul IslamDepartment of Tissue Engineering and Applied Cell Sciences, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Somayeh Ebrahimi-BaroughDepartment of Tissue Engineering and Applied Cell Sciences, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.ORCID 0000-0002-5234-4791
Tehran University of Medical Sciences · IRTarbiat Modares University · IRUniversity of Tehran · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GBM (Glioblastoma multiforme) is the  most prevalent and lethal primary brain tumor. Gene therapy is one of the promising approaches and  involves the delivery of genetic therapeutic molecules for specific antitumour response/activity. miRNAs can regulate the cell biology functions including replication, cell growth, and apoptosis by regulating gene expression. In this study, we found that down-regulation of miR-4731 expression occurred in GBM cells. We further determined that miR-4731 behaved as a tumor suppressor by inhibiting GBM cell proliferation. We further investigated the molecular mechanisms of miR-4731 and EGFR, ERK-1,2 and AKT-1,2 in GBM cell lines U87 and U251. The in vitro ectopic expression of miR-4731 affected cell proliferation, migration, and invasion of U87 and U251 cells. Luciferase reporter assays validated that miR-4731 targeted the 3'-untranslated region (3'-UTR) of EGFR. In conclusions, we identified that miR-4731 plays a tumor suppressor role in GBM cell proliferation and migration by targeting EGFR expression, and miR-4731 may act as a novel biomarker for early diagnosis or therapeutic target of GBM.

Indexed as

ApoptosisBiomarkers, TumorCell CycleCell MovementCell ProliferationErbB ReceptorsGene Expression Regulation, NeoplasticGlioblastomaHumansMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-aktTumor Cells, CulturedAKT1 protein, humanAKT2 protein, humanBiomarkers, TumorEGFR protein, humanErbB ReceptorsMAPK1 protein, humanMAPK3 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-aktApoptosisGlioblastomamiR-4731miRNAs

Identifiers

PMID33369441
PMCPMC8046313
OpenAlexW3117302083

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.