In this issue of Cancer Research, Xia and colleagues show that MYC-induced metabolic reprograming results in dependency on the serine-glycine-one-carbon (SGOC) metabolic pathway in neuroblastoma. This occurs through MYCN and ATF4 activation of the SGOC biosynthetic pathway in MYCN-amplified cells. Furthermore, inhibition of de novo serine synthesis generates metabolic stress in MYCN-amplified neuroblastoma cells, causing cell-cycle arrest and autophagy. Together, these data suggest that the SGOC pathway is an attractive therapy target in neuroblastoma.See related article by Xia et al., p. 3837.
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