Evidence map›Paper›PMID 40210802›Full record

ArticleClinical and experimental medicine2025

Isolation and characterization of extracellular vesicles from EGFR mutated lung cancer cells.

Dian Jamel Salih, Katrin S Reiners, Roberta Alfieri, Ahmed Mohammed Salih, Zulema Antonia Percario, Mariantonietta Di Stefano, Sollitto Francesco, Elisabetta Affabris, Gunther Hartmann, Teresa Santantonio

Abstract read
In one paragraph

Article in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. 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

10 authors.

Dian Jamel SalihDepartment of Medical and Surgical Sciences, University of Foggia, Via Napoli, 121, 71122, Foggia, Italy. dian.salih@unifg.it.
Katrin S ReinersInstitute of Clinical Chemistry and Clinical Pharmacology, University Hospital Bonn, Bonn, Germany.
Roberta AlfieriDepartment of Medicine and Surgery, University of Parma, Parma, Italy.
Ahmed Mohammed SalihCollege of Nursing, University of Duhok, Duhok, Iraq.
Zulema Antonia PercarioDepartment of Science, University Roma Tre, Rome, Italy.
Mariantonietta Di StefanoDepartment of Medical and Surgical Sciences, University of Foggia, Via Napoli, 121, 71122, Foggia, Italy.
Sollitto FrancescoDepartment of Medical and Surgical Sciences, University of Foggia, Via Napoli, 121, 71122, Foggia, Italy.
Elisabetta AffabrisDepartment of Science, University Roma Tre, Rome, Italy.
Gunther HartmannInstitute of Clinical Chemistry and Clinical Pharmacology, University Hospital Bonn, Bonn, Germany.
Teresa SantantonioDepartment of Medical and Surgical Sciences, University of Foggia, Via Napoli, 121, 71122, Foggia, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR) signaling pathway is essential for cellular processes such as proliferation, survival, and migration. Dysregulation of EGFR signaling is frequently observed in non-small cell lung cancer (NSCLC) and is associated with poor prognosis. This study aims to isolate and characterize extracellular vesicles (EVs) released by mutant EGFR lung cancer cell line PC9 and compare them with wild-type EGFR lung cancer cell line A549, while also evaluating the effect of gefitinib treatment on EV secretion and cargo composition. The two lung cancer cell lines were cultured with 2% EV-free serum, and EVs were subsequently isolated by differential ultra centrifugation. EVs were characterized by nanoparticle tracking analysis (NTA) and transmission electron microscopy (TEM) for quantification size and shape determination. Western blot analysis confirmed the enrichment and purity of isolated EVs. Results showed that EGFR mutation significantly increased EV release and altered their size, compared to EVs released by wild-type EGFR cells. In addition to classical EV markers such as CD81, Flotillin- 1, and TSG101, Western blot analysis also detected phosphorylated EGFR (p-EGFR) selectively packaged into EVs from PC9 cells. Gefitinib treatment significantly reduced EV secretion in PC9 cells and led to a marked decrease in p-EGFR incorporation into EVs, indicating that EV biogenesis and compostion are modulated by active EGFR signaling. In conclusion, this study highlights the significant influence of EGFR activation on EV secretion and cargo composition while demonstrating that EGFR inhibition via gefitinib alters EV-mediated signaling in lung cancer cells. These findings provide insights into tumor behavior, EV-mediated oncogenic communication, and the potential use of EVs as biomarkers and therapeutic targets in NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungErbB ReceptorsExtracellular VesiclesLung NeoplasmsMutationAntineoplastic AgentsCell Line, TumorGefitinibHumansAntineoplastic AgentsEGFR protein, humanErbB ReceptorsGefitinibEGFRExtracellular vesiclesLung cancer

Identifiers

PMID40210802
PMCPMC11985682

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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.