Claudin-4 as therapeutic target in cancer.

Abstract

BACKGROUND:

Intercellular junctional complexes such as adherens junctions and tight junctions are critical regulators of cellular polarity, paracellular permeability and metabolic and structural integrity of cellular networks. Abundant expression analysis data have yielded insights into the complex pattern of differentially expressed cell-adhesion proteins in epithelial cancers and provide a useful platform for functional, preclinical and clinical evaluation of novel targets.

SCOPE OF REVIEW:

This review will focus on the role of claudin-4, an integral constituent of tight junctions, in the pathophysiology of epithelial malignancies with particular focus pancreatic cancer, and its potential applicability for prognostic, diagnostic and therapeutic approaches.

MAJOR CONCLUSIONS:

Claudin-4 expression is widely dysregulated in epithelial malignancies and in a number of premalignant precursor lesions. Although the functional implications are only starting to unravel, claudin-4 seems to play an important role in tumour cell invasion and metastasis, and its dual role as receptor of Clostridium perfringens enterotoxin (CPE) opens exciting avenues for molecular targeted approaches.

GENERAL SIGNIFICANCE:

Claudin-4 constitutes a promising molecular marker for prognosis, diagnosis and therapy of epithelial malignancies.

• Authors: A Neesse, H Griesmann, T M Gress, P Michl
• Journal: Archives of biochemistry and biophysics (Arch Biochem Biophys) Vol. 524 Issue 1 Pg. 64-70 (Aug 01 2012) ISSN: 1096-0384 [Electronic] United States
• PMID: 22286027 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2012 Elsevier Inc. All rights reserved.

Chemical References

• CLDN4 protein, human
• Claudin-4
• Claudins

Topics

• Animals
• Carcinoma (drug therapy, genetics, metabolism, pathology)
• Claudin-4
• Claudins (genetics, metabolism)
• Drug Discovery
• Gene Expression Regulation, Neoplastic
• Humans
• Molecular Targeted Therapy (methods)
• Neoplasms (drug therapy, genetics, metabolism, pathology)
• Pancreas (drug effects, metabolism, pathology)
• Pancreatic Neoplasms (drug therapy, genetics, metabolism, pathology)
• Tight Junctions (drug effects, genetics, metabolism, pathology)