miR-181a mediates metabolic shift in colon cancer cells via the PTEN/AKT pathway

FEBS Lett. 2014 May 2;588(9):1773-9. doi: 10.1016/j.febslet.2014.03.037. Epub 2014 Mar 28.

Abstract

Cancer cell metabolism is often characterized by a shift from an oxidative to a glycolytic bioenergetics pathway, a phenomenon known as the warburg effect. Whether the deregulation of miRNAs contributes to the warburg effect remains largely unknown. Here we show that miR-181a expression is increased and thus induces a metabolic shift in colon cancer cells. miR-181a performs this function by inhibiting the expression of PTEN, leading to an increase of phosphorylated AKT which triggers metabolic shift. The increase of lactate production induced by miR-181a results in the rapid growth of cancer cells. These results identify miR-181a as a molecular switch involved in the orchestration of the warburg effect in colon cancer cells via the PTEN/AKT pathway.

Keywords: Glycolysis; PTEN; miR-181a.

MeSH terms

  • Cell Proliferation
  • Colonic Neoplasms
  • Gene Expression Regulation, Neoplastic*
  • HCT116 Cells
  • Humans
  • Lactic Acid / metabolism
  • MicroRNAs / physiology*
  • PTEN Phosphohydrolase / genetics
  • PTEN Phosphohydrolase / metabolism*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • RNA Interference
  • Signal Transduction
  • Transcriptome

Substances

  • MIrn181 microRNA, human
  • MicroRNAs
  • Lactic Acid
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • PTEN protein, human