Increase in intracellular PGE2 induces apoptosis in Bax-expressing colon cancer cells
By: Lisenn Lalier, Francois Pedelaborde, Christophe Braud, Jean Menanteau, Francois M Vallette and Christophe Olivier

BMC Cancer 2011, 11:153 doi:10.1186/1471-2407-11-153
Published: 27 April 2011

Abstract (Provisional)

Background

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.

Methods

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.

Results

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 either by PGE2 microinjection or by the pharmacological inhibition of PGE2 exportation and enzymatic degradation.

Conclusions

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.

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