Evidence map›Paper›PMID 32005873›Full record

ArticleScientific reports2020

miR-548x and miR-4698 controlled cell proliferation by affecting the PI3K/AKT signaling pathway in Glioblastoma cell lines.

Mohammad Reza Kalhori, Ehsan Arefian, Fereshteh Fallah Atanaki, Kaveh Kavousi, Masoud Soleimani

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

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  13. Targeting miRNA by Natural Products: A Novel Therapeutic Approach for Nonalcoholic Fatty Liver.Evidence-based complementary and alternative medicine : eCAM · 2021
    Review
  14. Article
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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

5 authors at 3 institutions in 1 country.

Mohammad Reza KalhoriMedical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.ORCID http://orcid.org/0000-0002-3652-0927
Ehsan ArefianMolecular Virology lab, Department of Microbiology, School of Biology, College of Science, University of Tehran, Tehran, Iran. arefian@ut.ac.ir.
Fereshteh Fallah AtanakiLaboratory of Complex Biological Systems and Bioinformatics (CBB), Department of Bioinformatics, Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran.
Kaveh KavousiLaboratory of Complex Biological Systems and Bioinformatics (CBB), Department of Bioinformatics, Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran.
Masoud SoleimaniDepartment of Hematology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
University of Tehran · IRKermanshah University of Medical Sciences · IRTarbiat Modares University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most aggressive and prevalent form of brain tumor cancers that originate from glial cells. This study proposed to investigate the effect of miR-548x and miR-4698 on the proliferation and the PI3K/AKT signaling pathway in glioblastoma cell lines. The molecular features of glioblastoma were studied using KEGG and TCGA sites. Next, by using miRwalk 2.0 and TargetScan version 7.1, the microRNAs that target critical genes in the PI3k/AKT pathway were selected according to score. The pre-miR-548x and pre-miR-4698 were cloned in a pCDH plasmid to produced lentiviral vector. The expression levels of miR-548x, miR-4698 and target genes were detected by qRT-PCR. The MTT, cell cycle, annexin and colony formation assay was used to detect the cell proliferation. MiR-548x and miR-4698 predicted target genes (Rheb, AKT1, mTOR, PDK1) were also evaluated by luciferase assay. The expression of AKT was detected by western blotting. Our results described that overexpression of miR-548x and miR-4698 could inhibit proliferation of A-172 and U251 cells. Also, miR-548x promoted the cell cycle arrest of GBM cell lines. The luciferase reporter assay results showed the 3' UTR of PDK1, RHEB, and mTOR are direct targets of the miR-548x and miR-4698. Too, the western blot analysis revealed that miR-548x and miR-4698 could downregulate the AKT1 protein expression. Overall, our findings suggest that miR-548x and miR-4698 could function as tumor suppressor genes in glioblastoma by controlling the PI3K/AKT signaling pathway and may act as gene therapy for clinical treatment of glioblastoma multiforme.

Indexed as

3' Untranslated RegionsBrain NeoplasmsCell Cycle CheckpointsCell Line, TumorCell ProliferationGlioblastomaHumansMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyruvate Dehydrogenase Acetyl-Transferring KinaseRas Homolog Enriched in Brain ProteinSignal TransductionTOR Serine-Threonine Kinases3' Untranslated RegionsMicroRNAsMIRN4698 microRNA, humanMIRN548 microRNA, humanMTOR protein, humanPDK1 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyruvate Dehydrogenase Acetyl-Transferring KinaseRas Homolog Enriched in Brain ProteinRHEB protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID32005873
PMCPMC6994486
OpenAlexW3003812463

What OpenQuestion holds

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LicenceCC BY
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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.