Evidence map›Paper›PMID 30483126›Full record

ArticleFrontiers in pharmacology2018

Low Expression of miR-466f-3p Sustains Epithelial to Mesenchymal Transition in Sonic Hedgehog Medulloblastoma Stem Cells Through Vegfa-Nrp2 Signaling Pathway.

Zein Mersini Besharat, Claudia Sabato, Agnese Po, Francesca Gianno, Luana Abballe, Maddalena Napolitano, Evelina Miele, Felice Giangaspero, Alessandra Vacca, Giuseppina Catanzaro and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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  11. The Non-coding Side of Medulloblastoma.Frontiers in cell and developmental biology · 2020
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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

11 authors at 3 institutions in 1 country.

Zein Mersini BesharatDepartment of Experimental Medicine, Sapienza University, Rome, Italy.
Claudia SabatoDepartment of Molecular Medicine, Sapienza University, Rome, Italy.
Agnese PoDepartment of Molecular Medicine, Sapienza University, Rome, Italy.
Francesca GiannoDepartment of Radiological, Oncological and Pathological Science, Sapienza University, Rome, Italy.
Luana AbballeDepartment of Experimental Medicine, Sapienza University, Rome, Italy.
Maddalena NapolitanoDepartment of Molecular Medicine, Sapienza University, Rome, Italy.
Evelina MieleDepartment of Hematology/Oncology and Stem Cell Transplantation, Bambino Gesù Children's Hospital, Istituto di Ricovero e Cura a Carattere Scientifico, Rome, Italy.
Felice GiangasperoDepartment of Radiological, Oncological and Pathological Science, Sapienza University, Rome, Italy.
Alessandra VaccaDepartment of Experimental Medicine, Sapienza University, Rome, Italy.
Giuseppina CatanzaroDepartment of Experimental Medicine, Sapienza University, Rome, Italy.
Elisabetta FerrettiDepartment of Experimental Medicine, Sapienza University, Rome, Italy.
Sapienza University of Rome · ITBambino Gesù Children's Hospital · ITItalian Institute of Technology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-throughput analysis has improved the knowledge of medulloblastoma (MB), the leading cause of cancer related death in children, allowing a better comprehension of the key molecular pathways in MB pathogenesis. However, despite these advances, 30% of patients still die from the disease and survivors face severe long-term side effects. Cancer stem cells (CSCs) represent a subset of cells that not only drive tumorigenesis, but are also one of the main determinants of chemoresistance. Epithelial mesenchymal transition (EMT) is a hallmark of cancer and up to now few data is available in MB. To give insight into the role of the EMT process in maintaining the mesenchymal phenotype of CSCs, we analyzed the expression of EMT related transcripts and microRNAs in these cells. We firstly isolated CSCs from Sonic Hedgehog (SHH) MB derived from Ptch1 heterozygous mice and compared their expression level of EMT-related transcripts and microRNAs with cerebellar NSCs. We identified two molecules linked to SHH and EMT, Vegfa and its receptor Nrp2, over-expressed in SHH MB CSCs. Inhibition of Vegfa showed impairment of cell proliferation and self-renewal ability of CSCs concurrent with an increase of the expression of the EMT gene, E-cadherin, and a decrease of the EMT marker, Vimentin. Moreover, among deregulated microRNAs, we identified miR-466f-3p, a validated inhibitor of both Vegfa and Nrp2. These results allowed us to describe a new EMT molecular network, involving the down-regulation of miR-466f-3p together with the concordant up-regulation of Vegfa and Nrp2, that sustains the mesenchymal phenotype of SHH MB CSCs.

Indexed as

epithelial to mesenchymal transitionmedulloblastomamiR-466f-3pNrp2sonic hedgehog medulloblastoma cancer stem cellsvegfa

Identifiers

PMID30483126
PMCPMC6240675
OpenAlexW2901131915

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.