Evidence map›Paper›PMID 24747968›Full record

ArticleOncogene2015

Two mature products of MIR-491 coordinate to suppress key cancer hallmarks in glioblastoma.

Xia Li, Yuexin Liu, Kirsi J Granberg, Qinhao Wang, Lynette M Moore, Ping Ji, Joy Gumin, Erik P Sulman, George A Calin, Hannu Haapasalo and 5 more

Abstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.0field-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

58 citing papers in PubMed, 98 citations in OpenAlex.

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  20. Bcl-xL: A Focus on Melanoma Pathobiology.International journal of molecular sciences · 2021
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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

15 authors at 4 institutions in 3 countries.

Xia Li *Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Yuexin Liu *Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Kirsi J GranbergDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Qinhao WangDepartment of Biochemistry and Molecular Biology, State Key Laboratory of Cancer Biology, The Fourth Military Medical University, Xi'an, China.
Lynette M MooreDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Ping JiDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Joy GuminDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Erik P SulmanDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
George A CalinDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Hannu HaapasaloDepartment of Pathology, Fimlab Laboratories and University of Tampere, Tampere, Finland.
Matti NykterDepartment of Signal Processing, Tampere University of Technology, Tampere, Finland.
Ilya ShmulevichInstitute for Systems Biology, Seattle, Washington, USA.
Gregory N FullerDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Frederick F LangDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Wei ZhangDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
The University of Texas MD Anderson Cancer Center · USTampere University · FIAir Force Medical University · CNInstitute for Systems Biology · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Tropism Enhanced Oncolytic Adenovirus for the Treatment of Brain TumorsP50CA127001 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Juan Fueyo · 2008 to 2026
$41.2M
Center for Systems Analysis of the Cancer RegulomeU24CA143835 · NCI · INSTITUTE FOR SYSTEMS BIOLOGY · PI SHMULEVICH, ILYA · 2009 to 2016
$10.6M
glioma Through Genomics and Transgenic Mouse ModelR01CA098503 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI FULLER, GREGORY NEAL, ZHANG, WEI · 2004 to 2014
$2.2M
Oncogene cooperation in glioma genesisR01CA141432 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FULLER, GREGORY NEAL, ZHANG, WEI · 2010 to 2014
$1.6M
Bone Marrow Stem Cells: Novel Treatment of Human GliomaR01CA115729 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LANG, FREDERICK F · 2006 to 2010
$1.3M
Dissecting Glioma Genesis through a Glial-Specific Mouse ModelR56CA098503 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FULLER, GREGORY NEAL, ZHANG, WEI · 2009 to 2009
$247k
NCI NIH HHS CA098503NCI NIH HHS CA115729NCI NIH HHS CA127001NCI NIH HHS CA141432NCI NIH HHS CA143835NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA127001NCI NIH HHS R01 CA098503NCI NIH HHS R01 CA115729NCI NIH HHS R01 CA141432NCI NIH HHS R56 CA098503NCI NIH HHS U24 CA143835
6 · The paper itself

Abstract

MIR-491 is commonly co-deleted with its adjacent CDKN2A on chromosome 9p21.3 in glioblastoma multiforme (GBM). However, it is not known whether deletion of MIR-491 is only a passenger event or has an important role. Small-RNA sequencing of samples from GBM patients demonstrated that both mature products of MIR-491 (miR-491-5p and -3p) are downregulated in tumors compared with the normal brain. The integration of GBM data from The Cancer Genome Atlas (TCGA), miRNA target prediction and reporter assays showed that miR-491-5p directly targets EGFR, CDK6 and Bcl-xL, whereas miR-491-3p targets IGFBP2 and CDK6. Functionally, miR-491-3p inhibited glioma cell invasion; overexpression of both miR-491-5p and -3p inhibited proliferation of glioma cell lines and impaired the propagation of glioma stem cells (GSCs), thereby prolonging survival of xenograft mice. Moreover, knockdown of miR-491-5p in primary Ink4a-Arf-null mouse glial progenitor cells exacerbated cell proliferation and invasion. Therefore, MIR-491 is a tumor suppressor gene that, by utilizing both mature forms, coordinately controls the key cancer hallmarks: proliferation, invasion and stem cell propagation.

Indexed as

Genes, Tumor SuppressorAnimalsbcl-X ProteinBrain NeoplasmsCell Line, TumorCyclin-Dependent Kinase 6ErbB ReceptorsGene Expression Regulation, NeoplasticGlioblastomaHumansInsulin-Like Growth Factor Binding Protein 2MaleMiceMicroRNAsNeoplasm Invasivenessbcl-X ProteinCDK6 protein, humanCyclin-Dependent Kinase 6ErbB ReceptorsInsulin-Like Growth Factor Binding Protein 2MicroRNAsMIRN491 microRNA, human

Identifiers

PMID24747968
PMCPMC4205227
OpenAlexW2048942013

What OpenQuestion holds

Textmetadata
LicenceTDM
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.