Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids
J. Clin. Invest. Isabelle M. Berquin, et al. 117:1866 doi:10.1172/JCI31494 [Go to this article.]

Figure 3
Pten deletion rate in mice on high–omega-3 and high–omega-6 diets. (A) Schematic representation of Pten and lacZ alleles before and after Cre-loxP–mediated recombination. In the ROSA26^LoxZ allele, recombination removes a sequence that interrupts the coding frame of β-galactosidase, resulting in activation of β-galactosidase enzyme. (B) Real-time quantification of Pten Δ5 allele. The inactive (exon 5 deletion) Pten allele and a control gene (wild-type Il-2) were quantified in 6-, 7-, and 8-week-old AP, DL, and VP lobes from mice on the high–omega-3 and high–omega-6 diet. Levels of the Pten Δ5 allele normalized to Il-2 are shown. Three mice were used for each data point, with bars representing SEM. Pten was deleted to similar extents in mice on either diet. (C) Prostates from 6-week-old Pten^loxP/loxPROSA26^Z/ZPB-cre4^T/– mice on the high–omega-3 and high–omega-6 diet were dissected, snap-frozen, and used for β-galactosidase staining as well as activity measurement. Three mice were used for each data point. Bars represent SEM. Pictures were taken at ×20 magnification. In 4 of the 6 mice that had sufficient protein remaining, the ratio of phosphorylated to total Akt, which is indicative of Pten inactivation, was quantified by Western blotting.