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Published on: July 25, 2017
Role of claudins in tumorigenesis
Karen Swisshelm1, Robert Macek, Manfred Kubbies
1Department of Pathology, Box 357470, University of Washington, Seattle, WA 98195-7470, USA. kswiss@u.washington.edu
Abstract:
The family of more than 20 claudin (CLDN) proteins comprises one of the major structural elements within the apical tight junction apparatus, a dynamic cellular nexus for maintenance of a luminal barrier, paracellular transport, and signal transduction. Loss of normal tight junction functions constitutes a hallmark of human carcinomas. CLDN1 may support tumor suppressive functions in tissues such as the brain, where dramatic loss of expression has been demonstrated in glioblastoma multiforme. The role(s) for CLDNs 3 and 4 in tumorigenesis is less clear. CLDN4 appears to be over-expressed in ovarian and pancreatic carcinomas, and this raises the possibility that a unique, potentially non-toxic cancer cell target may be developed through the design of enterotoxin analogues. Future goals include understanding the biochemical and physiological mechanisms that are perturbed as a consequence of CLDN alterations in the progression of solid tumors.
Insights
Claudins (CLDNs) are key to tight junctions, crucial for barrier function. Altered CLDN expression, particularly CLDN4 in cancers, suggests potential therapeutic targets for solid tumors.
Area of Science:
- Cell biology
- Oncology
- Molecular biology
Background:
- Claudins (CLDNs) are integral membrane proteins forming the tight junction, essential for cellular barrier function and transport.
- Disruption of tight junction integrity is a hallmark of human carcinomas.
- Specific claudin roles in tumorigenesis, like CLDN1's tumor suppressive function in brain cancers and CLDN4's overexpression in ovarian and pancreatic cancers, require further elucidation.
Purpose of the Study:
- To investigate the roles of claudins (CLDNs) in cancer progression.
- To explore the potential of CLDN4 as a therapeutic target in specific carcinomas.
Main Methods:
- Analysis of claudin expression patterns in various human cancers.
- Review of existing literature on claudin function in tight junctions and tumorigenesis.
Main Results:
- Claudin family proteins are critical structural components of the apical tight junction.
- Loss of claudin expression is observed in glioblastoma multiforme.
- Overexpression of CLDN4 is noted in ovarian and pancreatic carcinomas.
Conclusions:
- Claudin alterations are implicated in the progression of solid tumors.
- CLDN4 represents a potential target for novel cancer therapies, possibly through enterotoxin analogues.
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