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Increase in intracellular PGE2 induces apoptosis in Bax-expressing colon cancer cell. BMC Cancer 11:153

Département de Biologie Oncologique, Centre de Lutte Contre le Cancer René Gauducheau, Bd J, Monod, 44805 Nantes, Saint Herblain Cedex, France.
BMC Cancer (Impact Factor: 3.32). 04/2011; 11(1):153. DOI: 10.1186/1471-2407-11-153
Source: PubMed

ABSTRACT 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.

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Available from: Lisenn Lalier, Aug 16, 2015
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