[Lani]

from the article:
These mice carry the fat-1 gene from the roundworm Caenorhabditis elegans, encoding a n-3 PUFA desaturase, absent in mammals, that catalyzes conversion of n-6 into n-3 PUFA (22). Therefore, these mice have endogenously elevated n-3 PUFA tissue content and exhibit lower n-6/n-3 PUFA ratio compared to their wild-type (WT) littermates when maintained on a high n-6 PUFA diet. This contrasts feeding procedures using fish oil supplementation, which may bring confounding factors attributed in differences in the dietary composition. Hence, the fat-1 transgenic mouse model is a useful in vivo system for giving new insights of the role of n-6/n-3 fatty acid ratio in BC tumorigenesis.
...
When PGE2 has been shown to promote cancer development (51, 52) PGE3 has been found to have anticancer effects (53). Our results suggest that PGE3 and 17-HDHA might be anticancer metabolites, and these generated metabolites from EPA and DHA respectively may underlie the antitumor effect observed in the fat-1 transgenic mice. However, the concentration of PGE3 in the tumors of the fat-1 animals did not reach that of PGE2 suggesting that there is a role for AA-derived lipid mediators that cannot be totally replaced by EPA-derived lipid metabolites, EPA competing with AA acid as substrate for metabolite production. Interestingly, our in vitro experiments showed that addition of
14
17-HDHA downregulated HER2 and HER3 protein expression. Moreover, c-Myc expression was dramatically decreased by PGE2, PGE3 and 17-HDHA exposure.
These results suggest that PGE3 and 17-HDHA are anticancer mediators, and generation of PGE3 and 17-HDHA from n-3 PUFA may underlie the antitumor effect observed in fat-1 transgenic mice.