Connexins and Cadherin Crosstalk in the Pathogenesis of Prostate Cancer
Abstract
Gap junctions (GJ) are conglomerations of cell-cell channels that are formed by a family of 21 distinct proteins, called connexin (Cx)s. The Cxs are transmembrane proteins, which are designated according to molecular mass. They are assembled into GJs through many steps (Figure 1A). Communication through GJs is crucial for maintaining homeostasis [1;2]. Impaired, or loss of, Cx expression has been documented in the pathogenesis of various carcinomas [1;3-5]. Moreover, many studies have shown that over-expression of Cxs in tumor cells attenuates the malignant phenotype in vivo and in vitro, reverses the changes associated with epithelial to mesenchymal transformation (EMT), and induces differentiation [3;4;6]. For example,Cx32 is expressed in the liver, lung, and exocrine glands, and knock out studies have shown that the incidence of carcinogen-induced tumors in these mice is higher [7-9]. Moreover, mutations in several Cx genes have been characterized in inherited diseases associated with aberrant proliferation and differentiation [1;10]. These studies support the notion that Cxs act as tumor suppressors. Despite this the molecular mechanisms by which Cxs are assembled into GJs and how GJs are disassembled are poorly understood.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2015
- Accession Number
- AD1007375
Entities
People
- Parmender P Mehta
Organizations
- University of Nebraska Omaha