Trimming the fat in non-small cell lung cancer: a new small molecule inhibitor of acetyl-CoA carboxylase to target fatty acid synthesis
Amanda L. Davis, Steven J. Kridel
Abstract
Amanda L. Davis, Steven J. Kridel
Abstract
In the October 2016 issue of Nature Medicine , Svensson et al. demonstrate that acetyl-CoA carboxylase 1 (ACC1) is required for non-small cell lung cancer (NSCLC) growth in preclinical models and treatment with an allosteric ACC1 inhibitor, ND-646, suppresses NSCLC through fatty acid synthesis inhibition (1). This study provides answers to questions the cancer metabolism field has asked since the discovery that enzymes within the fatty acid synthesis pathway are overexpressed in cancer (2). Is de novo fatty acid synthesis required for tumors to develop and progress? And can enzymes in the pathway be successfully targeted for therapy?
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In the October 2016 issue of Nature Medicine , Svensson et al. demonstrate that acetyl-CoA carboxylase 1 (ACC1) is required for non-small cell lung cancer (NSCLC) growth in preclinical models and treatment with an allosteric ACC1 inhibitor, ND-646, suppresses NSCLC through fatty acid synthesis inhibition (1). This study provides answers to questions the cancer metabolism field has asked since the discovery that enzymes within the fatty acid synthesis pathway are overexpressed in cancer (2). Is de novo fatty acid synthesis required for tumors to develop and progress? And can enzymes in the pathway be successfully targeted for therapy?
Key concepts: Fatty acid synthesis, Acetyl-CoA carboxylase, Fatty acid synthase, Pyruvate carboxylase, Fatty acid metabolism, Enzyme, Fatty acid, Small molecule