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Perturbation of the tight junction permeability barrier by occludin loop peptides activates

I Vietor1, T Bader, K Paiha

  • 1IMP, Institute of Molecular Pathology, Dr. Bohrgasse 7, A-1030 Vienna, Austria.

EMBO Reports
|April 18, 2001
PubMed

Insights

Synthetic peptides targeting occludin disrupted tight junctions in mammary cells, leading to unpolarized clusters. This study reveals cross-talk between tight and adherens junctions, potentially driving oncogenesis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncogenesis

Background:

  • The integrity of epithelial barriers is crucial for tissue function and is maintained by cell junctions.
  • Tight junctions (TJs) and adherens junctions (AJs) play key roles in regulating cell polarity and tissue architecture.
  • Disruptions in junctional complexes are implicated in cancer progression.

Purpose of the Study:

  • To investigate the functional relationship between tight junctions (TJs) and adherens junctions (AJs) in mammary epithelial cells.
  • To determine the effect of occludin disruption on AJ signaling pathways.
  • To explore the potential role of TJ-AJ cross-talk in oncogenic transformation.

Main Methods:

  • Treatment of mouse mammary epithelial cells with synthetic peptides homologous to occludin's extracellular domain.
  • Assessment of occludin protein levels at tight junctions.
  • Analysis of cell morphology, polarization, and cluster formation.
  • Quantification of beta-catenin and c-myc gene and protein expression.
  • Transcriptional assays using a beta-catenin/TCF/LEF reporter construct.

Main Results:

  • Interference with occludin integrity disrupted the transepithelial permeability barrier.
  • Occludin-disrupting peptides reduced occludin at tight junctions, causing multilayered, unpolarized cell clusters.
  • Adherens junction protein beta-catenin transcription was induced, leading to increased beta-catenin/TCF/LEF transcriptional activity.
  • Occludin-II peptide treatment up-regulated the expression of the downstream target gene c-myc.

Conclusions:

  • A functional cross-talk exists between tight junctions and adherens junctions in mammary epithelial cells.
  • Disruption of tight junction integrity can trigger signaling pathways associated with adherens junctions.
  • This TJ-AJ cross-talk may contribute to the stepwise transformation of cells during oncogenesis.

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