How are the Arachidonate metabolites involved in carcinogenesis?
Favors cell proliferation via prostaglandin mechanism and cell membrane formation.
I am also very interested in this question! There are evidences that dietary n-3 PUFA inhibit progression of carcinogenesis by suppression of arachidonic acid – derived eicosanoid biosynthesis. Eicosanoids generated from AA, such as PGE2, leukotriene B4, thromboxane A2 and others were positively linked to carcinogenesis in their promotion of tumor cell survival and, additionally, they were found at higher concentrations in cancer cells than in normal cells. Also interesting is that the formation of AA-derived eicosanoids is decreased not only by n-3 PUFAs but also by eicosanoids derived from them, and some of these eicosanoids have an even more inhibitory effect. So, the ways to inhibit the generation of eicosanoids might be beneficial for treatment since they seem to interefere on many levels with the carcinogenic progression - production of ROS, inhibition of apoptosis, modulation of inflammation processes, proliferation, angiogenesis, etc..
Thank Maria Thomas for valuable information.
Is there any published paper relevant to this subject?
http://www.biomedcentral.com/content/pdf/1471-2407-12-606.pdf
http://www.lef.org/magazine/mag2007/feb2007_cover_prostate_01.htm
http://www.ncbi.nlm.nih.gov/pubmed/22349822
http://www.sciencedirect.com/science/article/pii/S0006291X97967991
Thank Michael J Gonzalez and Kit for your valuable information.
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