Gap junctions are essential communication conduits of astrocytes. Breaches of these ubiquitous networking channels are conceived to be a sinister method of metastatic proliferation in the central nervous system (CNS) by breast and lung carcinomas. In a recent study by Chen et al,1 the relationships and mechanisms between these gap junction–forming carcinomas and CNS metastasis were explored. In addition, Chen et al report interesting findings on what is delivered through these gap junctions that allows these carcinomas to proliferate and survive chemotherapeutic effects.
Astrocyte gap junctions, specifically named Cx43, allow astrocytes to communicate with each other. Perversely, it is also apparent that carcinomas can form these same gap junctions. This permits the potential for carcinomas to communicate with astrocytes through these channels. Chen et al1 report a proliferative presence of Cx43 at the interface between CNS-metastatic breast and lung carcinomas to normal astrocytes (Figure). Further analysis of the Cx43 gap junctions led the study investigators to believe that there exists an additional component that works in synergy with Cx43 to develop a carcinoma-astrocyte gap junction enfranchisement.
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