Evidence map›Paper›PMID 30845654›Full record

ReviewCancers2019

EMT Regulation by Autophagy: A New Perspective in Glioblastoma Biology.

Barbara Colella, Fiorella Faienza, Sabrina Di Bartolomeo

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
12.5field-weighted citation impact, top 1% 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

80 citing papers in PubMed, 135 citations in OpenAlex.

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20 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Barbara ColellaDepartment of Biosciences and Territory, University of Molise, 86090 Pesche (IS), Italy. b.colella@studenti.unimol.it.
Fiorella FaienzaDepartment of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. fiorella.faienza@uniroma2.it.ORCID 0000-0001-6148-0333
Sabrina Di BartolomeoDepartment of Biosciences and Territory, University of Molise, 86090 Pesche (IS), Italy. sabrina.dibartolomeo@unimol.it.
University of Molise · ITUniversity of Rome Tor Vergata · IT

Funding

Ministero dell'Istruzione, dell'Università e della Ricerca FFABR to Sabrina Di Bartolomeo
6 · The paper itself

Abstract

Epithelial-to-mesenchymal transition (EMT) and its reverse process MET naturally occur during development and in tissue repair in vertebrates. EMT is also recognized as the crucial event by which cancer cells acquire an invasive phenotype through the activation of specific transcription factors and signalling pathways. Even though glial cells have a mesenchymal phenotype, an EMT-like process tends to exacerbate it during gliomagenesis and progression to more aggressive stages of the disease. Autophagy is an evolutionary conserved degradative process that cells use in order to maintain a proper homeostasis, and defects in autophagy have been associated to several pathologies including cancer. Besides modulating cell resistance or sensitivity to therapy, autophagy also affects the migration and invasion capabilities of tumor cells. Despite this evidence, few papers are present in literature about the involvement of autophagy in EMT-like processes in glioblastoma (GBM) so far. This review summarizes the current understanding of the interplay between autophagy and EMT in cancer, with special regard to GBM model. As the invasive behaviour is a hallmark of GBM aggressiveness, defining a new link between autophagy and EMT can open a novel scenario for targeting these processes in future therapeutical approaches.

Indexed as

autophagycadherinsepithelial-to-mesenchymal transition (EMT)glioblastoma (GBM)Wnt/β-catenin signalling

Identifiers

PMID30845654
PMCPMC6468412
OpenAlexW2920675450

What OpenQuestion 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 OpenQuestion graph.