Metastasis is the most fatal complication in cancer patients. Upregulation of COX-2 and its downstream prostaglandins is usually observed in cancer patients and has been linked to metastasis. Some prostaglandins mechanisms have been already identified, but there are others whose roles remain elusive. Here, human cancer cells and a human breast cancer cell line overexpressing COX2 were used to evaluate the pro-migratory mechanisms of specific prostaglandins. The results showed that the inhibition of prostacyclin and prostaglandin synthases inhibited cell migration, which could be rescued by treating cancer cells with a prostacyclin analogue. Moreover, only pharmacological IP receptor knockdown decreased cell migration and expression of pro-migratory genes in COX2 expressing human breast cancer cells, which matched with the enhanced migration in cancer cells with IP-activated receptors. Finally, the IP-dependent signalling pathway was identified to activate pro-migratory genes in COX2 overexpressing human breast cancer cells. Overall, the researchers elucidate signalling mechanisms of pro-migratory behaviour through prostacyclin IP receptor activation in COX2 overexpressing breast cancer cells that could lead to novel therapeutic targets to hinder tumor progression.
Pro-migratory actions of the prostacyclin receptor in human breast cancer cells that over-express cyclooxygenase-2
Nenad Petrovic(1), Michael Murray(2), Sarah E Allison(2)
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