Figure 6. Mechanisms through which an inhibition of stearoyl-CoA desaturase (SCD) by some pharmaceuticals can cause potent anti-tumor effects.

Such inhibition elicits a rise of cellular concentrations of acyl-CoA esters of saturated fatty acids and a concomitant decline of cellular concentrations of acyl-CoA esters of unsaturated fatty acids. Genes, proteins and processes whose increased expression levels, activities and rates promote tumorigenesis in cells that are not exposed to the SCD inhibitors are displayed in red color. Proteins and processes whose activities and rates attenuate tumorigenesis in response to cell treatment with the SCD inhibitors are displayed in green color. See text for more details. Abbreviations: ACC, acetyl-CoA carboxylase; AMPK, AMP-activated protein kinase; Akt, a serine/threonine-specific protein kinase; ER, endoplasmic reticulum; FA-CoA, acyl-CoA ester of fatty acid; FASN, fatty acid synthase; PI3K/Akt, phosphatidylinositol-3 kinase/Akt signaling pathway; PM, plasma membrane; SREBP, sterol regulatory element-binding protein; UPR^ER, the unfolded protein response signaling pathway in the ER.