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Updated: Jul 31, 2026

A Modified In vitro Invasion Assay to Determine the Potential Role of Hormones, Cytokines and/or Growth Factors in Mediating Cancer Cell Invasion
06:36

A Modified In vitro Invasion Assay to Determine the Potential Role of Hormones, Cytokines and/or Growth Factors in Mediating Cancer Cell Invasion

Published on: April 24, 2015

Signaling mechanisms that mediate invasion in prostate cancer cells

L Bonaccorsi1, S Marchiani, M Muratori

  • 1Dipartimento di Fisiopatologia Clinica (Unità di Andrologia), University of Florence, Italy.

Annals of the New York Academy of Sciences
|January 15, 2005
PubMed

Insights

Androgen receptor expression in prostate cancer cells reduces epidermal growth factor receptor (EGFR) signaling, decreasing cell invasion. This suggests potential therapeutic strategies targeting EGFR for androgen-independent prostate cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Androgen-sensitive prostate cancer cells exhibit reduced migration and invasion.
  • The role of androgen receptors (AR) in modulating epidermal growth factor receptor (EGFR) signaling is not fully understood.

Purpose of the Study:

  • To investigate how androgen receptor presence affects EGFR-mediated signaling pathways in prostate cancer cells.
  • To evaluate the impact of AR on EGFR autophosphorylation and downstream PI3K/AKT pathway activation.
  • To assess the therapeutic potential of EGFR inhibition in androgen-independent prostate cancer.

Main Methods:

  • Immunoprecipitation studies to assess EGFR tyrosine phosphorylation.
  • Measurement of PI3K activity in response to EGF stimulation.
  • In vitro invasion assays using Matrigel.
  • Treatment with gefitinib (EGFR inhibitor) and R1881 (androgen agonist).

Main Results:

  • PC3 cells transfected with AR (PC3-AR) showed reduced EGF-induced EGFR tyrosine phosphorylation.
  • EGF-stimulated PI3K activity was decreased in PC3-AR cells and further reduced by R1881.
  • Gefitinib inhibited EGFR autotransphosphorylation and PI3K activation in androgen-insensitive cell lines (PC3, DU145), reducing in vitro invasion.

Conclusions:

  • Androgen receptor expression confers a less malignant phenotype by interfering with EGFR signaling and reducing invasion.
  • EGFR inhibition using gefitinib can decrease invasion and proliferation in androgen-independent prostate cancer.
  • Targeting EGFR may be a viable strategy for treating advanced prostate cancer.

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