Evidence map›Paper›PMID 32823532›Full record

ArticleCancers2020

mTOR Inhibition Leads to Src-Mediated EGFR Internalisation and Degradation in Glioma Cells.

Barbara Colella, Mayra Colardo, Gianna Iannone, Claudia Contadini, Cristina Saiz-Ladera, Claudia Fuoco, Daniela Barilà, Guillermo Velasco, Marco Segatto, Sabrina Di Bartolomeo

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Sialylation Inhibition Impairs Migration and Promotes Adhesion of GBM Cells.International journal of molecular sciences · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Targeting RTK-PI3K-mTOR Axis in Gliomas: An Update.International journal of molecular sciences · 2021
    Review
  10. Article
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

10 authors at 3 institutions in 2 countries.

Barbara ColellaDepartment of Biosciences and Territory, University of Molise, 86090 Pesche (IS), Italy.
Mayra ColardoDepartment of Biosciences and Territory, University of Molise, 86090 Pesche (IS), Italy.
Gianna IannoneDepartment of Biosciences and Territory, University of Molise, 86090 Pesche (IS), Italy.
Claudia ContadiniDepartment of Biology, University of RomeTor Vergata, 00133 Rome, Italy.
Cristina Saiz-LaderaDepartment of Biochemistry and Molecular Biology, School of Biology, Complutense University and Instituto de Investigaciones Sanitarias San Carlos (IdISSC), 28040 Madrid, Spain.
Claudia FuocoDepartment of Biology, University of RomeTor Vergata, 00133 Rome, Italy.ORCID 0000-0001-8372-305X
Daniela BarilàDepartment of Biology, University of RomeTor Vergata, 00133 Rome, Italy.
Guillermo VelascoDepartment of Biochemistry and Molecular Biology, School of Biology, Complutense University and Instituto de Investigaciones Sanitarias San Carlos (IdISSC), 28040 Madrid, Spain.
Marco SegattoDepartment of Biosciences and Territory, University of Molise, 86090 Pesche (IS), Italy.ORCID 0000-0003-0465-9470
Sabrina Di BartolomeoDepartment of Biosciences and Territory, University of Molise, 86090 Pesche (IS), Italy.ORCID 0000-0002-5748-1541
University of Molise · ITUniversity of Rome Tor Vergata · ITInstituto de Investigación Sanitaria del Hospital Clínico San Carlos · ES

Funding

European Regional Development Fund (ERDF) I2013-2016Instituto de Salud Carlos III (ISCIII) PI18/00442Ministero dell'Istruzione, dell'Università e della Ricerca FFABR
6 · The paper itself

Abstract

Epidermal Growth Factor receptor (EGFR) is a tyrosine kinase receptor widely expressed on the surface of numerous cell types, which activates several downstream signalling pathways involved in cell proliferation, migration and survival. EGFR alterations, such as overexpression or mutations, have been frequently observed in several cancers, including glioblastoma (GBM), and are associated to uncontrolled cell proliferation. Here we show that the inhibition of mammalian target of Rapamycin (mTOR) mediates EGFR delivery to lysosomes for degradation in GBM cells, independently of autophagy activation. Coherently with EGFR internalisation and degradation, mTOR blockade negatively affects the mitogen activated protein/extracellular signal-regulated kinase (MAPK)/ERK pathway. Furthermore, we provide evidence that Src kinase activation is required for EGFR internaliation upon mTOR inhibition. Our results further support the hypothesis that mTOR targeting may represent an effective therapeutic strategy in GBM management, as its inhibition results in EGFR degradation and in proliferative signal alteration.

Indexed as

autophagyEGFRgliomamTOR

Identifiers

PMID32823532
PMCPMC7464593
OpenAlexW3048912410

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.