GPR35 risk variant for PSC enhances cellular metabolism and proliferation

Genetic variations in G protein–coupled receptor 35 (GPR35) are associated with an increased risk for primary sclerosing cholangitis (PSC) and related cancers however the general function of GPR35 is poorly understood.

Using Gpr35-deficient mice, we found that GPR35 promotes the activity of sodium/potassium-ATPase, a ubiquitous and essential transmembrane pump that regulates cellular metabolism and proliferation.

A genetic variant of GPR35 associated with PSC heightens sodium/potassium-ATPase activity, enhancing glycolysis and proliferation of intestinal epithelial cells compared to non-PSC-associated GPR35.

Intriguingly, treatment reducing GPR35 activity decreased tumor burden in mice suggesting that GPR35 could be an attractive target for the treatment of PSC and related cancers.

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