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Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation
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Sortilin exhibits tumor suppressor-like activity by limiting EGFR transduction function.

E Lapeyronnie1, C Granet1, J Tricard1,2

  • 1UMR Inserm 1308 CAPTuR, Contrôle de l'Activation cellulaire, Progression Tumorale et Résistance thérapeutique and Chaire de Pneumologie Expérimentale, Université de Limoges, Faculté de Médecined, Limoges, CEDEX, France.

Oncogene
|February 14, 2026
PubMed
Summary
This summary is machine-generated.

Sortilin, a protein regulating cytoplasmic epidermal growth factor receptor (EGFR), may act as a tumor suppressor in lung cancer. Its expression could predict how well anti-EGFR therapies will work.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Lung cancer is a leading cause of cancer death globally, often driven by mutated epidermal growth factor receptor (EGFR).
  • While EGFR inhibitors show initial promise, therapeutic resistance frequently develops, limiting long-term efficacy.
  • EGFR functions as a transcription factor, promoting oncogenic drivers that contribute to treatment resistance.

Purpose of the Study:

  • To investigate the role of sortilin in regulating EGFR signaling and its potential impact on lung cancer.
  • To explore the relationship between sortilin, EGFR, and oncogenic drivers like cMYC.
  • To determine if sortilin expression can predict patient response to anti-EGFR therapies.

Main Methods:

  • Utilized genome-wide chromatin binding assays to identify interactions between sortilin and EGFR.
  • Analyzed the binding of sortilin to gene regulatory elements, including those associated with cMYC.
  • Correlated sortilin expression levels with the efficacy of anti-EGFR therapies in lung adenocarcinoma models.

Main Results:

  • Sortilin was identified as a regulator of cytoplasmic EGFR, attenuating its signal transduction.
  • Sortilin was found to interact with gene regulatory elements occupied by EGFR.
  • Sortilin also binds to regulatory elements of cMYC, suggesting a tumor suppressor-like function.
  • Sortilin expression levels showed potential as a predictive biomarker for anti-EGFR therapy response.

Conclusions:

  • Sortilin plays a role in modulating EGFR activity and may possess tumor suppressor functions in lung cancer.
  • The interaction of sortilin with EGFR and cMYC regulatory elements provides a molecular mechanism for its activity.
  • Sortilin expression is a potential predictive biomarker for the efficacy of anti-EGFR treatments in lung adenocarcinoma.