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An Agrin-YAP/TAZ Rigidity Sensing Module Drives EGFR-Addicted Lung Tumorigenesis.

Reza Bayat Mokhtari1, Divyaleka Sampath2, Paige Eversole1

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|April 1, 2025
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Summary
This summary is machine-generated.

Epidermal growth factor receptor (EGFR) senses tissue rigidity by dictating tumorigenic agrin expression in lung cancer. This agrin-EGFR axis, linked to YAP-TEAD, offers a therapeutic strategy for EGFR-driven lung cancers.

Keywords:
EGFR, extracellular matrixYAP/TAZagrinhippo pathwaylung cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biophysics

Background:

  • Epidermal growth factor receptor (EGFR) is a key oncogene in lung adenocarcinoma (LUAD).
  • The role of extracellular matrix (ECM) rigidity in cancer development is increasingly recognized.
  • Mechanisms by which EGFR senses ECM rigidity are not well understood.

Purpose of the Study:

  • To investigate how EGFR senses ECM rigidity in lung cancer.
  • To elucidate the role of agrin in EGFR-mediated mechanotransduction.
  • To identify potential therapeutic strategies targeting the EGFR-ECM interaction in LUAD.

Main Methods:

  • Analysis of EGFR-driven lung cancer cell lines, genetically engineered mouse models, and human specimens.
  • Investigation of agrin expression and its functional role in EGFR-reliant cancer cells.
  • Mechanistic studies on agrin-mediated EGFR activation and its interaction with integrin β1.
  • Exploration of the interplay between EGFR-agrin signaling and YAP-TEAD mechanosensing.

Main Results:

  • EGFR dictates tumorigenic agrin expression in lung cancer.
  • Agrin confers substrate stiffness-dependent oncogenic properties to EGFR-reliant cancer cells.
  • Agrin mechanoactivates EGFR via EGF-dependent and independent pathways, interacting with integrin β1.
  • A feed-forward loop between agrin-EGFR and YAP-TEAD is crucial for tumorigenesis.

Conclusions:

  • EGFR senses ECM rigidity through agrin-mediated mechanotransduction.
  • The agrin-EGFR-YAP/TEAD axis represents a critical pathway in EGFR-driven lung tumorigenesis.
  • Combined inhibition of EGFR and YAP/TEAD may be a viable therapeutic strategy for lung cancers addicted to EGFR.