Connexins in Prostate Cancer Initiation and Progression
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 transmembrane proteins and are designated according to molecular mass. They are assembled into GJs through many steps (Figure 1). 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 GJs are assembled and disassembled are poorly understood.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2012
- Accession Number
- ADA581406
Entities
People
- Parmender P Mehta
Organizations
- University of Nebraska–Lincoln