Evidence map›Paper›PMID 26437223›Full record

ArticleOncotarget2015

miR-135b suppresses tumorigenesis in glioblastoma stem-like cells impairing proliferation, migration and self-renewal.

Valentina Lulli, Mariachiara Buccarelli, Maurizio Martini, Michele Signore, Mauro Biffoni, Stefano Giannetti, Liliana Morgante, Giovanna Marziali, Ramona Ilari, Alfredo Pagliuca and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-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

29 citing papers in PubMed, 50 citations in OpenAlex.

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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

14 authors at 2 institutions in 1 country.

Valentina LulliDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Mariachiara BuccarelliDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Maurizio MartiniInstitute of Anatomic Pathology, Università Cattolica del Sacro Cuore, Rome, Italy.
Michele SignoreDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Mauro BiffoniDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Stefano GiannettiInstitute of Human Anatomy, Università Cattolica del Sacro Cuore, Rome, Italy.
Liliana MorganteInstitute of Human Anatomy, Università Cattolica del Sacro Cuore, Rome, Italy.
Giovanna MarzialiDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Ramona IlariDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Alfredo PagliucaDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Luigi Maria LaroccaInstitute of Anatomic Pathology, Università Cattolica del Sacro Cuore, Rome, Italy.
Ruggero De MariaRegina Elena National Cancer Institute, Rome, Italy.
Roberto PalliniInstitute of Neurosurgery, Università Cattolica del Sacro Cuore, Rome, Italy.
Lucia Ricci-VitianiDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Istituto Superiore di Sanità · ITUniversità Cattolica del Sacro Cuore · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most common and fatal malignant adult primary brain tumor. Currently, the overall prognosis for GBM patients remains poor despite advances in neurosurgery and adjuvant treatments. MicroRNAs (miRNAs) contribute to the pathogenesis of various types of tumor, including GBM. In this study we analyzed the expression of a panel of miRNAs, which are known to be differentially expressed by the brain and GBM tumor, in a collection of patient-derived GBM stem-like cells (GSCs). Notably, the average expression level of miR-135b, was the most downregulated compared to its normal counterpart, suggesting a potential role as anti-oncogene.Restoration of miR-135b in GSCs significantly decreased proliferation, migration and clonogenic abilities. More importantly, miR-135b restoration was able to significantly reduce brain infiltration in mouse models of GBM obtained by intracerebral injection of GSC lines. We identified ADAM12 and confirmed SMAD5 and GSK3β as miR-135b targets and potential mediators of its effects. The whole transcriptome analysis ascertained that the expression of miR-135b downmodulated additional genes driving key pathways in GBM survival and infiltration capabilities.Our results identify a critical role of miR-135b in the regulation of GBM development, suggesting that miR-135b might act as a tumor-suppressor factor and thus providing a potential candidate for the treatment of GBM patients.

Indexed as

Cell MovementCell ProliferationCell Self RenewalADAM12 ProteinADAM ProteinsAnimalsApoptosisCell Line, TumorDown-RegulationGene Expression ProfilingGene Expression Regulation, NeoplasticGenotypeGlioblastomaGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHeterograftsADAM12 ProteinADAM12 protein, humanADAM ProteinsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseMembrane ProteinsMicroRNAsMIRN135 microRNA, humanSmad5 ProteinADAM12glioblastoma stem cellsGSK3βmiRNAsSMAD5

Identifiers

PMID26437223
PMCPMC4741927
OpenAlexW2284890769

What OpenQuestion holds

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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 OpenQuestion graph.