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EGFR modulates complement activation in head and neck squamous cell carcinoma.

Anas H A Abu-Humaidan1,2, Lars Ekblad3, Johan Wennerberg4

  • 1Division of Infection Medicine, Department of Clinical Sciences, Lund University, Lund, Sweden. A.abuHumaidan@ju.edu.jo.

BMC Cancer
|February 15, 2020
PubMed
Summary

Epidermal growth factor receptor (EGFR) influences the complement system in head and neck squamous cell carcinoma (HNSCC). EGFR inhibition in HNSCC increases complement activation, impacting treatment response and side effects.

Keywords:
Cancer microenvironmentComplement activationComplement regulationEGFRHNSCCIressaTyrosine kinase inhibitor

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Area of Science:

  • Oncology
  • Immunology
  • Cell Biology

Background:

  • Epidermal growth factor receptor (EGFR) is crucial for epithelial cell growth and is overexpressed in cancers like head and neck squamous cell carcinoma (HNSCC).
  • EGFR signaling impacts innate immune functions in epithelia, with a known role in modulating the complement system in skin.

Purpose of the Study:

  • To investigate the role of EGFR in modulating the complement system specifically within HNSCC.
  • To understand how EGFR inhibition affects complement activation in HNSCC.

Main Methods:

  • Utilized patient-derived HNSCC cell lines with varying sensitivities to EGFR inhibitors.
  • Generated EGFR inhibition-resistant HNSCC cell lines for comparative analysis.

Main Results:

  • HNSCC cell lines activate the complement system upon incubation with human serum.
  • Complement activation increased in EGFR inhibitor-sensitive cell lines treated with the tyrosine kinase inhibitor Iressa.
  • EGFR-inhibitor resistant cell lines showed complement activation and reduced complement regulatory proteins, even without inhibitors.
  • Complement activation did not lead to HNSCC cell lysis but increased extracellular signal-regulated kinase (ERK) phosphorylation in one cell line.

Conclusions:

  • EGFR plays a significant role in modulating the complement system in HNSCC.
  • Prolonged EGFR inhibition in sensitive HNSCC cells enhances complement activation.
  • Findings have implications for understanding EGFR inhibitor efficacy, resistance mechanisms, and inflammatory side effects like skin lesions, which often lead to treatment discontinuation.