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: 3.36). 04/2011; 11(1):153. DOI: 10.1186/1471-2407-11-153
Source: PubMed


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
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    • "In mitochondria mediated apoptotic cell death process Bax acts as an essential gatekeeper as its activation irreversibly commits the most of the cells to die [40,41]. It has been studied extensively on its relationship with different types of cancer, such as  pancreatic [19,42], bladder [21], gastric [18], colorectal [43,44], esophageal [16], lung [32,45,46], cervical [47], colon [48,49], prostate carcinoma [50,51], squamous cell carcinoma of the head and neck [36], nasopharyngeal carcinoma [52], breast carcinomas [32,53], ovarian carcinoma [54], renal and transitional cell cancer [55], gliomas [56], CLL [30,31,33–35,38,57], Hodgkin’s lymphoma [17], non-Hodgkin's lymphoma [58], myeloma [59], acute leukemia [60], etc. Bax promoter contains response elements for an important tumor suppressor p53 and this affects gene expression [28]. With respect to the important roles of Bax in apoptosis, it is biologically plausible that its polymorphism may modulate the risk of cancer. "
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