Evidence map›Paper›PMID 33302515›Full record

ReviewCells2020

Cooperation and Interplay between EGFR Signalling and Extracellular Vesicle Biogenesis in Cancer.

Laura C Zanetti-Domingues, Scott E Bonner, R Sumanth Iyer, Marisa L Martin-Fernandez, Veronica Huber

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Exosome: an overview on enhanced biogenesis by small molecules.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  4. Article
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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

5 authors at 3 institutions in 2 countries.

Laura C Zanetti-DominguesCentral Laser Facility, Research Complex at Harwell, Rutherford Appleton Laboratory, Didcot OX11 0FA, UK.ORCID 0000-0003-0514-3185
Scott E BonnerThe Wood Lab, Department of Paediatrics, University of Oxford, Oxford OX1 3QX, UK.ORCID 0000-0003-2361-9968
R Sumanth IyerCentral Laser Facility, Research Complex at Harwell, Rutherford Appleton Laboratory, Didcot OX11 0FA, UK.ORCID 0000-0003-0418-2158
Marisa L Martin-FernandezCentral Laser Facility, Research Complex at Harwell, Rutherford Appleton Laboratory, Didcot OX11 0FA, UK.ORCID 0000-0001-5496-6300
Veronica HuberUnit of Immunotherapy of Human Tumors, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy.ORCID 0000-0001-6304-3575
Rutherford Appleton Laboratory · GBFondazione IRCCS Istituto Nazionale dei Tumori · ITUniversity of Oxford · GB

Funding

Biotechnology and Biological Sciences Research Council BB/M011224/1
6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) takes centre stage in carcinogenesis throughout its entire cellular trafficking odyssey. When loaded in extracellular vesicles (EVs), EGFR is one of the key proteins involved in the transfer of information between parental cancer and bystander cells in the tumour microenvironment. To hijack EVs, EGFR needs to play multiple signalling roles in the life cycle of EVs. The receptor is involved in the biogenesis of specific EV subpopulations, it signals as an active cargo, and it can influence the uptake of EVs by recipient cells. EGFR regulates its own inclusion in EVs through feedback loops during disease progression and in response to challenges such as hypoxia, epithelial-to-mesenchymal transition and drugs. Here, we highlight how the spatiotemporal rules that regulate EGFR intracellular function intersect with and influence different EV biogenesis pathways and discuss key regulatory features and interactions of this interplay. We also elaborate on outstanding questions relating to EGFR-driven EV biogenesis and available methods to explore them. This mechanistic understanding will be key to unravelling the functional consequences of direct anti-EGFR targeted and indirect EGFR-impacting cancer therapies on the secretion of pro-tumoural EVs and on their effects on drug resistance and microenvironment subversion.

Indexed as

Disease ProgressionEndocytosisEpithelial-Mesenchymal TransitionErbB ReceptorsExtracellular VesiclesHumansNeoplasmsSignal TransductionTetraspaninsTumor MicroenvironmentEGFR protein, humanErbB ReceptorsTetraspaninsendocytosisepidermal growth factor receptor (EGFR)EV biogenesisEV heterogeneityextracellular vesicles (EVs)microenvironment subversionMVB heterogeneitytherapy resistancetumour microenvironment

Identifiers

PMID33302515
PMCPMC7764760
OpenAlexW3110795491

What Socratic 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 Socratic graph.