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Open Access Research article

Increase in intracellular PGE2 induces apoptosis in Bax-expressing colon cancer cell

Lisenn Lalier12*, François Pedelaborde2, Christophe Braud2, Jean Menanteau2, François M Vallette2 and Christophe Olivier23

Author Affiliations

1 Département de Biologie Oncologique, Centre de Lutte Contre le Cancer René Gauducheau, Bd J. Monod, 44805 Nantes, Saint Herblain Cedex, France

2 Département de Recherche en Cancérologie, Université de Nantes, INSERM U892, 8 quai Moncousu, 44035 Nantes Cedex, France

3 Laboratoire de Toxicologie, Faculté de Pharmacie, Université de Nantes, 1 rue Gaston Veil, 44000 Nantes, France

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BMC Cancer 2011, 11:153  doi:10.1186/1471-2407-11-153

Published: 27 April 2011



NSAIDs exhibit protective properties towards some cancers, especially colon cancer. Yet, it is not clear how they play their protective role. PGE2 is generally shown as the only target of the NSAIDs anticancerous activity. However, PGE2 known targets become more and more manifold, considering both the molecular pathways involved and the target cells in the tumour. The role of PGE2 in tumour progression thus appears complex and multipurpose.


To gain understanding into the role of PGE2 in colon cancer, we focused on the activity of PGE2 in apoptosis in colon cancer cell lines.


We observed that an increase in intracellular PGE2 induced an apoptotic cell death, which was dependent on the expression of the proapoptotic protein Bax. This increase was induced by increasing PGE2 intracellular concentration, either by PGE2 microinjection or by the pharmacological inhibition of PGE2 exportation and enzymatic degradation.


We present here a new sight onto PGE2 in colon cancer cells opening the way to a new prospective therapeutic strategy in cancer, alternative to NSAIDs.