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. Author manuscript; available in PMC: 2012 Sep 1.
Published in final edited form as: Eur J Lipid Sci Technol. 2011 Nov;113(11):1321–1331. doi: 10.1002/ejlt.201100030

Figure 7.

Figure 7

Possible interrelationship between PUFAs metabolism and cell viability: PUFAs inhibition of PMPMEase probably contributes to a natural equilibrium between methylated (PMP) and unmethylated (PP) polyisoprenylated proteins. COX-2 expression in tumors results in the conversion of PUFAs to PGs, the loss of the PMPMEase inhibitory potency and a shift in the equilibrium in favor of PP and cell proliferation. This may explain why long term use of NSAIDs and consumption of PUFAs-rich foods may owe their anticancer benefits to the increased tissue levels of PUFAs and the resulting PMPMEase inhibition.