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      Gap junctions and connexins as therapeutic targets in cancer.

      Expert opinion on therapeutic targets
      Animals, antagonists & inhibitors, MicroRNAs, Apoptosis, Bystander Effect, Antineoplastic Agents, agonists, Humans, pharmacology, Gene Expression Regulation, Neoplastic, Gap Junctions, physiology, Neoplasm Metastasis, drug therapy, Tumor Markers, Biological, metabolism, Protein Processing, Post-Translational, Connexins, Genetic Therapy, drug effects, Connexin 43, genetics, Neoplasms, Cell Communication, physiopathology, therapy

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          Abstract

          Connexins (Cxs) and gap junctional intercellular communications (GJICs) play roles in cancer development, growth and metastasis. Experimental studies suggest that targeting Cxs may be a novel technique, either to inhibit tumor cell growth directly or to sensitize to various therapies. A brief introduction to the role of Cxs in cancer. The focus is mainly on data available in the literature regarding therapeutic aspects. This article reviews the various strategies that take advantage of gap junctions and connexins to eliminate cancer cells, including use of the bystander effect (BE) in gene therapy, the effect of connexins on chemosensitization, the role of apoptotic processes and interactions with the microenvironment. Attempts to restore connexin expression at the transcriptional and post-transcriptional levels are described, as well as promising strategies recently explored. The potential and limitations of the approaches are discussed. Connexins have multiple facets, singly, in hemichannel complexes, in gap junctions or interacting with different proteins. The regulation of their expression is not fully resolved and selective manipulation of Cxs expression is therefore a challenge. Although the therapeutic potential of connexins is undeniable, more effort is needed to study the regulation and functions of these proteins.

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