LINC00152/miR-139-5p regulates gastric cancer cell aerobic glycolysis by targeting PRKAA1

Biomed Pharmacother. 2018 Jan:97:1296-1302. doi: 10.1016/j.biopha.2017.11.015. Epub 2017 Dec 14.

Abstract

Gastric cancer is one of the most common cancers in the world and glycolysis is a major feature of gastric cancer. MicroRNAs (miRNAs) involve in gastric cancer cell proliferation, glycolysis and other cellular processes. MiR-139-5p is reported as a tumor suppressor in cancers, however, the role of miR-139-5p including glycolytic metabolism is unclear in gastric cancer. So, the purpose of the present study is to elucidate the underlying mechanism in gastric cancer metabolism mediated by miR-139-5p. Our results revealed that miR-139-5p inhibited glycolysis by regulating AMP-activated, alpha 1 catalytic subunit (PRKAA1) expression in gastric cancer cells. We also found that miR-139-5p was down-regulated by long intergenic non-coding RNA 152 (LINC00152) in gastric cancer cells. Our results indicate that LINC00152/miR-139-5p facilitates gastric cancer cell glycolysis by regulating PRKAA1 expression.

Keywords: Gastric cancer; Glycolysis; LINC00152; MiR-139-5p; PRKAA1.

MeSH terms

  • AMP-Activated Protein Kinases / genetics*
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Down-Regulation
  • Glycolysis / genetics*
  • Humans
  • RNA, Long Noncoding / genetics*
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / pathology

Substances

  • RNA, Long Noncoding
  • long non-coding RNA Linc00152, human
  • AMP-Activated Protein Kinases
  • PRKAA1 protein, human