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Background  Epithelial-to-mesenchymal transition (EMT) results in changes that promote de-differentiation, migration, and invasion in non-small cell lung cancer (NSCLC). While it is recognized that EMT promotes altered energy utilization, identification of metabolic pathways that link EMT with cancer progression is needed. Work presented here indicates that mesenchymal NSCLC upregulates glutamine-fructose-6-phosphate transaminase 2 (GFPT2). GFPT2 is the rate-limiting enzyme in the synthesis of uridine diphosphate  N -acetylglucosamine (UDP-GlcNAc). UDP-GlcNAc is the obligate activator of O-linked N-acetylglucosamine transferase (OGT).    Methods  Analysis of our transcriptomic data indicates that  GFPT2  is one of the most significantly upregulated metabolic genes in mesenchymal NSCLC. Ectopic GFPT2 expression, as well as gene silencing strategies were used to determine the importance of this metabolic enzyme in regulating EMT-driven processes of cell motility and invasion.    Results  Our work demonstrates that  GFPT2  is transcriptionally upregulated by NF-κB and repressed by the NAD + -dependent deacetylase SIRT6. Depletion of  GFPT2  expression in NSCLC highlights its importance in regulating cell migration and invasion during EMT.    Conclusions  Consistent with GFPT2 promoting cancer progression, we find that elevated  GFPT2  expression correlates with poor clinical outcome in NSCLC. Modulation of GFPT2 activity offers a potentially important therapeutic target to combat NSCLC disease progression.Electronic supplementary material  The online version of this article (10.1186/s12964-019-0335-5) contains supplementary material, which is available to authorized users.

NF-κB upregulates glutamine-fructose-6-phosphate transaminase 2 to promote migration in non-small cell lung cancer