Fig 1: Effect of 17ß-HSD12 on cancer cell proliferation. a Every elongation round of LCFAs consists of four steps. During the first step, the elongases of very long-chain fatty acids (ELOVL1–7) condense malonyl-CoA with a substrate fatty acyl-CoA. Subsequently, 3-ketoacyl-CoA reductase (KAR or 17ß-HSD12) reduces the 3-ketoacyl-CoA to 3-hydroxyacyl-CoA, which is then subjected to dehydration by 3-hydroxyacyl-CoA dehydratases (HACD1–4). A final reduction step is performed by 2,3-trans-enoyl-CoA reductase (TER) to yield a fatty acyl-CoA elongated by two carbon atoms. b The essential PUFAs linoleic acid and a-linolenic acid give rise to a wide array of ?-6 and ?-3 FAs, respectively, through a series of elongation and/or desaturation reactions. Fatty acid desaturases (FADS1 and FADS2) and ELOVLs (ELOVL2 and ELOVL5) with distinct substrate preferences participate at different steps of this metabolic pathway. The ?-6 osbond acid (22:5) and ?-3 docosahexaenoic acid (DHA, 22:6) are produced via elongation and desaturation of docosatetraenoic acid (DTA) and docosapentaenoic acid (DPA), respectively, followed by ß-oxidation in peroxisomes. c MCF7, MDA-MB-453, SUM159, and MDA-MB-231 cells were transfected with mock or 17ß-HSD12 siRNA or left untreated (ctrl). (Left panel) Live measurements of cell proliferation were performed with the xCELLigence RTCA DP instrument. The cell index values (average and standard deviation of four technical replicates) from one out of three independent experiments are shown. For the SUM159 cells, the cell index was normalized to 5 h to account for small differences in seeding in this experiment. (Right panel) At 24 h, 48 h, and 72 h post-transfection with siRNAs, cell nuclei were stained with Hoechst-33342 and analyzed by high-content imaging. The values represent the mean and error bars SD from at least three independent experiments per cell line, and are normalized to the mock siRNA samples at each time point (*p < 0.05, ***p < 0.001, ns not significant)