Targeting the elevated rate of de novo fatty acid synthesis (FASyn), which often occurs in tumour cells, has emerged as a promising therapeutic strategy. However, efforts to inhibit acetyl-CoA carboxylase (ACC) — the rate-limiting enzyme in FASyn — have so far been unsuccessful. Svensson et al. now show that ACC1 is highly expressed in human non-small-cell lung cancer (NSCLC) cell lines and that activity of this enzyme maintains NSCLC cell growth and viability in vitro and in vivo. Chronic treatment of xenograft and genetically engineered mouse models of NSCLC with the small-molecule allosteric ACC inhibitor ND-646 significantly inhibited tumour growth.
References
Svensson, R. U. et al. Inhibition of acetyl-CoA carboxylase suppresses fatty acid synthesis and tumor growth of non-small-cell lung cancer in preclinical models. Nat. Med. 22, 1108–1119 (2016)
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Crunkhorn, S. ACC inhibition suppresses lung cancer. Nat Rev Drug Discov 15, 750 (2016). https://doi.org/10.1038/nrd.2016.219
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DOI: https://doi.org/10.1038/nrd.2016.219
