Loss of FADS2 Causes Unusual Fatty Acid Synthesis Figure 2. GC results of FADS2 transfected MCF7 cells with 20:2n26 (8,11–20:2) and 20:3n23 (8,11,14–20:3) fatty acids. A: FADS1- transfected cells D5-desaturate 20:2n26R5,11,14–20:3 and 20:3n23R5,11,14,17–20:4. B: FADS2 transfected cells D8-desaturate 20:2n26R20:3n26 and 20:3n23R20:4n23. doi:10.1371/journal.pone.0028186.g002 as to long chain PUFA levels [19,20]. Further studies are needed to fully understand the consequences of FADS gene function loss and/or modulation based on SNPs in neoplasm. Early studies demonstrated that micro-cell mediated transfer of HSA11 into MCF7 cells reduced tumorigenicity, suggestive of potential tumor suppressor genes on this chromosome [21]. Our findings show that a primary molecular defect in MCF7 cells lies within the FADS2 gene causing loss of FADS2-encoded D6-desaturase activity. Compensation for FADS2 function by FADS1 leads to the production of 5,11,14–20:3 and 5,11,14,17– 20:4, both primarily dead-end fatty acid products that cannot be precursors for most eicosanoids and are likely to be competitive Figure 3. n26 LCPUFA pathway in MCF7 cells. D6- and D8-desaturation steps are absent in MCF7, leading to D5-desaturation of 11,14–20:2 to 5,11,14–20:3 when FADS1 is functional. The analogous pathways for n–3 LCPUFA convert 11,14,17–20:3R5,11,14,17–20:4 (not shown). FADS2 is also believed to be involved in C22 LCPUFA biosynthesis (not shown). doi:10.1371/journal.pone.0028186.g003 PLoS ONE | www.plosone.org 3 November 2011 | Volume 6 | Issue 11 | e28186