Related Experiment Video
Updated: Mar 14, 2026
Tension Gauge Tether Probes for Quantifying Growth Factor Mediated Integrin Mechanics and Adhesion
Published on: February 11, 2022
Epidermal growth factor receptor targeting alters gene expression and restores the adhesion function of cancerous
Shohreh Azadi1, Mohammad Tafazzoli-Shadpour2, Ramin Omidvar3,4,5
1Faculty of Biomedical Engineering, Amirkabir University of Technology (Tehran Polytechnic), No. 424, Hafez Avenue, Tehran, P.O. Box 15875-4413, Iran.
Abstract:
Loss of cell-cell adhesion function is a common characteristic of many human epithelial carcinomas that is frequently due to loss of E-cadherin expression. In cancer progression, loss of E-cadherin is associated with invasion and metastasis potential, hence restoration of its function may contribute to the metastasis inhibition. This study examined effect of Epidermal Growth Factor Receptor (EGFR/Her1) blockade on the E-cadherin expression, cellular adherence, and cell elasticity in two human epithelial cancer cell lines, MCF7 and A431. EGFR blocking agents as antibodies or small molecules target EGFR directly. Furthermore, due to intracellular signaling pathways they influence cell behavior and activities. The idea here is to investigate the effect of reduced activity of this signaling pathway using anti-EGFR Antibody (Cetuximab) and tyrosine kinase inhibitor (Lapatinib) on cell-cell adhesion and cell mechanical properties. Real-Time PCR analysis demonstrated that treatment of cells with considered drugs increased the expression of E-cadherin gene among samples. The atomic force microscopy-based single cell force spectroscopy technique was used to measure adhesive force of cancerous cells. Results indicated that inhibition of EGFR activity elevated cell-cell adhesion force, accompanied by stiffening of the cell bodies. In summary, Cetuximab and Lapatinib have been found to mediate cell-cell adhesion by restoration of E-cadherin expression and function. Our data suggest possible therapeutic potential for inhibition of metastasis via the blockade of EGFR signaling.
Insights
Blocking Epidermal Growth Factor Receptor (EGFR) with Cetuximab or Lapatinib restores E-cadherin expression, enhancing cell adhesion and potentially inhibiting cancer metastasis.
Area of Science:
- Oncology
- Cell Biology
- Biophysics
Background:
- Loss of E-cadherin expression impairs cell-cell adhesion in epithelial carcinomas, promoting cancer invasion and metastasis.
- Epidermal Growth Factor Receptor (EGFR) signaling pathways influence cell behavior, including adhesion and mechanical properties.
Purpose of the Study:
- To investigate the impact of blocking EGFR signaling on E-cadherin expression, cell-cell adhesion, and cell elasticity in human epithelial cancer cell lines.
- To evaluate the therapeutic potential of anti-EGFR agents in restoring cell adhesion and inhibiting metastasis.
Main Methods:
- Treatment of MCF7 and A431 cancer cell lines with anti-EGFR antibody (Cetuximab) and tyrosine kinase inhibitor (Lapatinib).
- Real-Time PCR to quantify E-cadherin gene expression.
- Atomic Force Microscopy (AFM)-based single-cell force spectroscopy to measure cell-cell adhesion force and cell elasticity.
Main Results:
- EGFR blockade significantly increased E-cadherin gene expression in both cell lines.
- Inhibition of EGFR activity enhanced cell-cell adhesion force.
- Cancer cells exhibited increased stiffness (elasticity) upon EGFR inhibition.
Conclusions:
- Cetuximab and Lapatinib restore E-cadherin expression and function, leading to increased cell-cell adhesion.
- Blocking EGFR signaling presents a potential therapeutic strategy for inhibiting cancer metastasis by improving cell adhesion and mechanical properties.
