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Review

The role of connexins in breast cancer: from misregulated cell communication to aberrant intracellular signaling

ORCID Icon, ORCID Icon, ORCID Icon & ORCID Icon
Article: 1962698 | Received 20 Apr 2021, Accepted 22 Jul 2021, Published online: 06 Aug 2021

Figures & data

Figure 1. Connexins and gap junction organizations. Six connexins oligomerize to form connexons (hemichannels) that can be either homomeric or heteromeric if they are formed from one type or more than one type of connexins, respectively. After the transport of connexons to the plasma membrane, they can function as non-junctional hemichannels or align with another connexon to complete the formation of either homotypic gap junction channels composed of the same type of connexon or heterotypic gap junctions consisting of different hemichannels.

Figure 1. Connexins and gap junction organizations. Six connexins oligomerize to form connexons (hemichannels) that can be either homomeric or heteromeric if they are formed from one type or more than one type of connexins, respectively. After the transport of connexons to the plasma membrane, they can function as non-junctional hemichannels or align with another connexon to complete the formation of either homotypic gap junction channels composed of the same type of connexon or heterotypic gap junctions consisting of different hemichannels.

Figure 2. Diverse roles of connexins in the primary and metastatic breast cancers. Connexins and GJIC were downregulated in primary breast cancers while elevation of Cx26, Cx32 and Cx43 expression was observed at metastatic sites of breast cancers. These effects can be regulated either through gap junction/hemichannel activities by modulating the exchange of molecules or channel-independent roles of connexins by interacting with several molecules in the cytosol or on the plasma membrane.

Figure 2. Diverse roles of connexins in the primary and metastatic breast cancers. Connexins and GJIC were downregulated in primary breast cancers while elevation of Cx26, Cx32 and Cx43 expression was observed at metastatic sites of breast cancers. These effects can be regulated either through gap junction/hemichannel activities by modulating the exchange of molecules or channel-independent roles of connexins by interacting with several molecules in the cytosol or on the plasma membrane.

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