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Researchers in Department of Physiology, Anatomy and Genetics have identified a rescue mechanism that allows cancers to overcome the consequences of inactivating mutations in critically important genes.

Co-culture of DLD1 cells loaded with spectrally-distinct fluorescent dyes, showing mixing of colours due to exchange across gap junctions.
Co-culture of DLD1 cells loaded with spectrally-distinct fluorescent dyes, showing mixing of colours due to exchange across gap junctions. This mechanism also exchanges small-molecule metabolites across the cellular network.

Gene mutations can give rise to cancer if they offer a survival advantage, such as a means of overcoming normal checks on growth. Over time, such mutations are positively selected and become enriched in human tumours. Indeed, many of these mutations are used to diagnose cancers. 

Since gene mutations are random, not all are advantageous and some may even be harmful to cancer cells by inactivating critically-important pathways. Previous in vitro studies have identified multiple metabolic pathways that are essential for cancer cell growth, and proposed that blocking these would be therapeutic. A prediction borne from these studies is that loss-of-function mutations in essential genes should undergo negative selection, and thus not appear in human cancers. However, the phenomenon of negative selection is exceedingly rare in human cancers. This paradox suggests that cancer cells are somehow protected from inactivating mutations in critically important pathways. Researchers in Department of Physiology, Anatomy and Genetics's (DPAG) Swietach group researchers have now described a mechanism that may underpin this rescue of cancerous cells.

In their study, cancer cells that were made deficient in certain enzymatic or transport activities could have their phenotype ‘rescued’ by gaining access to wild-type proteins in neighbouring cells. This rescue occurs through the exchange of solutes across gap junctions, and Cx26 emerges as a particularly important gap junctional channel.  Thus, a syncytial network of cancer cells can be protected from spontaneously inactivating mutations in certain critical genes.

Read the full story on the DPAG website

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