As part of a shift toward macromolecule production to support continuous cell proliferation,
cancer cells coordinate the activation of
lipid biosynthesis and the signaling networks that stimulate this process. A ubiquitous metabolic event in
cancer is the constitutive activation of the
fatty acid biosynthetic pathway, which produces
saturated fatty acids (SFAs) and
monounsaturated fatty acids (MUFAs) to sustain the increasing demand of new membrane
phospholipids with appropriate acyl composition. In
cancer cells, the tandem activation of the
fatty acid biosynthetic
enzymes adenosine triphosphate citrate lyase,
acetyl-CoA carboxylase (ACC) and
fatty acid synthase (FAS) leads to increased synthesis of SFA and their further conversion into MUFA by
stearoyl-CoA desaturase (SCD) 1. The roles of
adenosine triphosphate citrate lyase, ACC and FAS in the pathogenesis of
cancer have been a subject of extensive investigation. However, despite early experimental and epidemiological observations reporting elevated levels of MUFA in
cancer cells and tissues, the involvement of SCD1 in the mechanisms of
carcinogenesis remains surprisingly understudied. Over the past few years, a more detailed picture of the functional relevance of SCD1 in cell proliferation, survival and transformation to
cancer has begun to emerge. The present review addresses the mounting evidence that argues for a key role of SCD1 in the coordination of the intertwined pathways of
lipid biosynthesis, energy sensing and the transduction signals that influence mitogenesis and
tumorigenesis, as well as the potential value of this
enzyme as a target for novel pharmacological approaches in
cancer interventions.