Dlx-2 and glutaminase upregulate epithelial-mesenchymal transition and glycolytic switch

Oncotarget. 2016 Feb 16;7(7):7925-39. doi: 10.18632/oncotarget.6879.

Abstract

Most cancer cells depend on enhanced glucose and glutamine (Gln) metabolism for growth and survival. Oncogenic metabolism provides biosynthetic precursors for nucleotides, lipids, and amino acids; however, its specific roles in tumor progression are largely unknown. We previously showed that distal-less homeobox-2 (Dlx-2), a homeodomain transcription factor involved in embryonic and tumor development, induces glycolytic switch and epithelial-mesenchymal transition (EMT) by inducing Snail expression. Here we show that Dlx-2 also induces the expression of the crucial Gln metabolism enzyme glutaminase (GLS1), which converts Gln to glutamate. TGF-β and Wnt induced GLS1 expression in a Dlx-2-dependent manner. GLS1 shRNA (shGLS1) suppressed in vivo tumor metastasis and growth. Inhibition of Gln metabolism by shGLS1, Gln deprivation, and Gln metabolism inhibitors (DON, 968 and BPTES) prevented Dlx-2-, TGF-β-, Wnt-, and Snail-induced EMT and glycolytic switch. Finally, shDlx-2 and Gln metabolism inhibition decreased Snail mRNA levels through p53-dependent upregulation of Snail-targeting microRNAs. These results demonstrate that the Dlx-2/GLS1/Gln metabolism axis is an important regulator of TGF-β/Wnt-induced, Snail-dependent EMT, metastasis, and glycolytic switch.

Keywords: Dlx-2; GLS1; Snail; epithelial-mesenchymal transition; glycolytic switch.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Apoptosis
  • Blotting, Western
  • Cell Proliferation
  • Chromatin Immunoprecipitation
  • Epithelial-Mesenchymal Transition*
  • Fluorescent Antibody Technique
  • Glutaminase / antagonists & inhibitors
  • Glutaminase / genetics
  • Glutaminase / metabolism*
  • Glutamine / metabolism*
  • Glycolysis / physiology*
  • HeLa Cells
  • Hep G2 Cells
  • Homeodomain Proteins / antagonists & inhibitors
  • Homeodomain Proteins / genetics
  • Homeodomain Proteins / metabolism*
  • Humans
  • MCF-7 Cells
  • Neoplasms / genetics
  • Neoplasms / metabolism
  • Neoplasms / pathology*
  • RNA, Messenger / genetics
  • Real-Time Polymerase Chain Reaction
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • Snail Family Transcription Factors / antagonists & inhibitors
  • Snail Family Transcription Factors / genetics
  • Snail Family Transcription Factors / metabolism
  • Transcription Factors / antagonists & inhibitors
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Transforming Growth Factor beta / antagonists & inhibitors
  • Transforming Growth Factor beta / genetics
  • Transforming Growth Factor beta / metabolism
  • Tumor Cells, Cultured

Substances

  • Distal-less homeobox proteins
  • Homeodomain Proteins
  • RNA, Messenger
  • Snail Family Transcription Factors
  • Transcription Factors
  • Transforming Growth Factor beta
  • Glutamine
  • Adenosine Triphosphate
  • GLS protein, human
  • Glutaminase