SREBP1-Induced Glutamine Synthetase Triggers a Feedforward Loop to Upregulate SREBP1 through Sp1 O-GlcNAcylation and Augments Lipid Droplet Formation in Cancer Cells

Int J Mol Sci. 2021 Sep 10;22(18):9814. doi: 10.3390/ijms22189814.

Abstract

Glutamine and lipids are two important components of proliferating cancer cells. Studies have demonstrated that glutamine synthetase (GS) boosts glutamine-dependent anabolic processes for nucleotide and protein synthesis, but the role of GS in regulating lipogenesis remains unclear. This study identified that insulin and glutamine deprivation activated the lipogenic transcription factor sterol regulatory element-binding protein 1 (SREBP1) that bound to the GS promoter and increased its transcription. Notably, GS enhanced the O-linked N-acetylglucosaminylation (O-GlcNAcylation) of the specificity protein 1 (Sp1) that induced SREBP1/acetyl-CoA carboxylase 1 (ACC1) expression resulting in lipid droplet (LD) accumulation upon insulin treatment. Moreover, glutamine deprivation induced LD formation through GS-mediated O-GlcNAc-Sp1/SREBP1/ACC1 signaling and supported cell survival. These findings demonstrate that insulin and glutamine deprivation induces SREBP1 that transcriptionally activates GS, resulting in Sp1 O-GlcNAcylation. Subsequently, O-GlcNAc-Sp1 transcriptionally upregulates the expression of SREBP1, resulting in a feedforward loop that increases lipogenesis and LD formation in liver and breast cancer cells.

Keywords: O-GlcNAcylation; cancer; glutamine synthetase; lipid droplet; sterol regulatory element-binding protein 1.

MeSH terms

  • Acetyl-CoA Carboxylase / genetics*
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / pathology
  • Cell Proliferation / genetics
  • Gene Expression Regulation, Neoplastic / genetics
  • Glutamate-Ammonia Ligase / genetics*
  • Glutamine / metabolism
  • Humans
  • Insulin / metabolism
  • Lipids / genetics
  • Liver Neoplasms / genetics*
  • Liver Neoplasms / metabolism
  • Liver Neoplasms / pathology
  • Metabolism / genetics
  • Promoter Regions, Genetic / genetics
  • Protein Biosynthesis / genetics
  • Signal Transduction
  • Sp1 Transcription Factor / genetics*
  • Sterol Regulatory Element Binding Protein 1 / genetics*
  • beta-N-Acetylhexosaminidases / genetics

Substances

  • Insulin
  • Lipids
  • SREBF1 protein, human
  • Sp1 Transcription Factor
  • SP1 protein, human
  • Sterol Regulatory Element Binding Protein 1
  • Glutamine
  • hexosaminidase C
  • beta-N-Acetylhexosaminidases
  • glutamine synthetase I
  • Glutamate-Ammonia Ligase
  • ACACA protein, human
  • Acetyl-CoA Carboxylase