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Comment
. 2018 Apr 1;32(7-8):463-465.
doi: 10.1101/gad.315168.118.

Acetyl-CoA-directed gene transcription in cancer cells

Inmaculada Martínez-Reyes  1 , Navdeep S Chandel  1
Affiliations
Comment

Acetyl-CoA-directed gene transcription in cancer cells

Inmaculada Martínez-Reyes et al. Genes Dev. .

Abstract

Fluctuations in acetyl-coenzyme A (acetyl-CoA) levels have been previously associated with changes in global histone acetylation and gene expression. The study by Lee and colleagues (pp. 497-511) in this issue of Genes & Development demonstrates that acetyl-CoA can promote the up-regulation of cell migration- and adhesion-related genes in glioblastoma by controlling Ca2+-NFAT (nuclear factor of activated T cells) signaling.

Keywords: NFAT1; acetyl-CoA; calcium; glioblastoma; histone acetylation; metabolism.

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Figures

Figure 1.
Figure 1.
Acetyl-CoA promotes cell migration and adhesion by controlling Ca2+–NFAT (nuclear factor of activated T cells) signaling. Acetyl-CoA is produced by the oxidative decarboxylation of pyruvate from glycolysis and enters the TCA cycle. Citrate is released from mitochondria and converted to acetyl-CoA by ACLY. Acetate generates acetyl-CoA by ACSS2. High levels of acetyl-CoA promote an increased influx of calcium into the cells, activating and translocating NFAT to the nucleus. In combination with p300, NFAT drives site-specific regulation of H3K27 acetylation (H3K27ac) and increases the expression of genes related to cell migration and adhesion to the ECM.
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