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Modulation of cell adhesion molecules in various epithelial cell lines after treatment with PP2

Anna Maria Calcagno1, Jennifer M Fostel, Randal P Orchekowski

  • 1Department of Pharmaceutical Chemistry, The University of Kansas, Lawrence, Kansas 66047, USA. calcagnoa@mail.nih.gov

Molecular Pharmaceutics
|June 7, 2005
PubMed

Insights

Inhibiting Src tyrosine kinases with PP2 increases E-cadherin, enhancing cell adhesion and barrier function in epithelial cells. This suggests a key role for Src kinases in regulating epithelial integrity.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • E-cadherin is crucial for epithelial barrier function and paracellular permeability.
  • Src family tyrosine kinases are implicated in regulating cell adhesion and epithelial integrity.

Purpose of the Study:

  • To investigate the effect of PP2, a Src tyrosine kinase inhibitor, on E-cadherin expression and function in various epithelial cell lines.
  • To determine how Src inhibition impacts cell morphology, adhesion, and paracellular permeability.

Main Methods:

  • Treatment of epithelial cell lines (HCT-116, HT29, Caco-2, LS174T, ARPE-19) with 20 microM PP2.
  • Assessment of morphological changes, cell clustering, and E-cadherin localization via microscopy.
  • Measurement of transepithelial electrical resistance to evaluate paracellular permeability.
  • Analysis of E-cadherin and Claudin 3 protein and mRNA expression levels.

Main Results:

  • PP2 treatment induced cell clustering and E-cadherin redistribution to cell contacts in Caco-2, HT29, and HCT-116 cells.
  • Transepithelial electrical resistance increased in Caco-2 cells, indicating enhanced barrier function.
  • E-cadherin protein levels increased in most cell lines, except HCT-116; ARPE-19 cells lacked E-cadherin expression.
  • Claudin 3 mRNA expression significantly increased in intestinal cell lines.

Conclusions:

  • Inhibition of Src tyrosine kinases by PP2 positively regulates E-cadherin at functional and protein expression levels.
  • Src inhibition enhances E-cadherin-dependent cell adhesion and improves epithelial barrier function.
  • These findings highlight the role of Src kinases in maintaining epithelial integrity through E-cadherin modulation.

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