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Prostaglandin E 2  (PGE 2 ) is associated with proliferation and angiogenesis in colorectal tumours. The role of prostaglandin transporter OATP2A1/ SLCO2A1  in colon cancer tumorogenesis is unknown. We evaluated mice of various  Slco2a1  genotypes in a murine model of colon cancer, the adenomatous polyposis (APC) mutant ( Apc    ∆716/ + ) model. Median lifespan was significantly extended from 19 weeks in  Slco2a1   +/+ / Apc    Δ716/ +  mice to 25 weeks in  Slco2a1   −/− / Apc    Δ716/ +  mice. Survival was directly related to a reduction in the number of large polyps in the  Slco2a1   −/−   /Apc    ∆716/ +  compared to the  Slco2a1   +/+ / Apc    Δ716/ +  or  Slco2a1   +/− / Apc    Δ716/ + mice. The large polyps from the  Slco2a1   −/−   /Apc    ∆716/ +  mice had significant reductions in microvascular density, consistent with the high expression of  Slco2a1  in the tumour-associated vascular endothelial cells. Chemical suppression of OATP2A1 function significantly reduced tube formation and wound-healing activity of PGE 2  in human vascular endothelial cells (HUVECs) although the amount of extracellular PGE 2  was not affected by an OATP2A1 inhibitor. Further an  in vivo  model of angiogenesis, showed a significant reduction of haemoglobin content (54.2%) in sponges implanted into  Slco2a1   −/− , compared to wildtype mice. These studies indicate that OATP2A1 is likely to promote tumorogenesis by PGE 2  uptake into the endothelial cells, suggesting that blockade of OATP2A1 is an additional pharmacologic strategy to improve colon cancer outcomes.

A novel role for OATP2A1/SLCO2A1 in a murine model of colon cancer