Increase in intracellular PGE(2 )induces apoptosis in Bax-expressing colon cancer cell

BACKGROUND: NSAIDs exhibit protective properties towards some cancers, especially colon cancer. Yet, it is not clear how they play their protective role. PGE(2 )is generally shown as the only target of the NSAIDs anticancerous activity. However, PGE(2 )known targets become more and more manifold, considering both the molecular pathways involved and the target cells in the tumour. The role of PGE(2 )in tumour progression thus appears complex and multipurpose. METHODS: To gain understanding into the role of PGE(2 )in colon cancer, we focused on the activity of PGE(2 )in apoptosis in colon cancer cell lines. RESULTS: We observed that an increase in intracellular PGE(2 )induced an apoptotic cell death, which was dependent on the expression of the proapoptotic protein Bax. This increase was induced by increasing PGE(2 )intracellular concentration, either by PGE(2 )microinjection or by the pharmacological inhibition of PGE(2 )exportation and enzymatic degradation. CONCLUSIONS: We present here a new sight onto PGE(2 )in colon cancer cells opening the way to a new prospective therapeutic strategy in cancer, alternative to NSAIDs.