Increase in intracellular PGE2 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. PGE2 is generally shown as the only target of the NSAIDs anticancerous activity.

Dietary prevention of malignant glioma aggressiveness, implications in oxidant stress and apoptosis.

Our study explored the influence of diet on gliomagenesis and associated systemic effects (SE) in rats. The experimental diet contained various ingredients supposed to interfere with carcinogenesis, mainly phytochemicals (PtcD for phytochemical diet) and its effects were compared to those of the same diet without the phytochemicals (BD for basal diet). Glioma was induced by ethylnitrosourea to pregnant females fed the diets from the start of gestation until the moment of sacrifice of the offpsrings.

Increase in PGE2 biosynthesis induces a Bax dependent apoptosis correlated to patients' survival in glioblastoma multiforme.

Prostaglandin E(2) plays multiple roles both in the physiology and the physiopathology of human brain, which are not completely understood. We have identified in a subset of human glioblastoma multiforme (GBM) tumors, the most common form of adult brain cancer, an increased expression of mPGES-1, the enzyme which catalyses the isomerization of PGH(2) into PGE(2) downstream of cyclooxygenase 2 (COX-2). The sensitivity of primary cultures of GBM to apoptosis was augmented by the overexpression of mPGES-1, whereas the knockdown of its expression by shRNA decreased the apoptotic threshold in vitro and stimulated tumor growth in vivo.