PPARα Promotes Cancer Cell Glut1 Transcription Repression

J Cell Biochem. 2017 Jun;118(6):1556-1562. doi: 10.1002/jcb.25817. Epub 2017 Jan 5.

Abstract

Abundant nutrient availability including glucose and amino acids plays an important role in maintaining cancer cell energetic and biosynthetic pathways. As a nuclear receptor, peroxisome-proliferator-activated receptor α (PPARα) regulates inflammation and cancer progression, however, it is still unclear the interaction of PPARα with the cancer cell glucose metabolism. Here we found that PPARα reduced Glut1 (Glucose transporter 1) protein and gene levels in HCT-116, SW480, HeLa, and MCF-7 cancer cell lines. In contrast, silenced PPARα reversed this event. Further analysis shows that PPARα directly targeted the consensus PPRE motif of Glut1 promoter region resulting in Glut1 transcription repression. PPARα-mediated Glut1 transcription repression led to decreased influx of glucose in cancer cells. These findings revealed a novel mechanism of PPARα-mediated cancer cell Glut1 transcription repression. J. Cell. Biochem. 118: 1556-1562, 2017. © 2016 Wiley Periodicals, Inc.

Keywords: CELL SIGNALING; GLUT1; PPARα; TRANSCRIPTION REPRESSION.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Down-Regulation*
  • Gene Expression Regulation, Neoplastic
  • Glucose / metabolism
  • Glucose Transporter Type 1 / genetics*
  • Glucose Transporter Type 1 / metabolism
  • HCT116 Cells
  • HeLa Cells
  • Humans
  • MCF-7 Cells
  • Neoplasms / genetics
  • Neoplasms / metabolism*
  • PPAR alpha / metabolism*
  • Promoter Regions, Genetic

Substances

  • Glucose Transporter Type 1
  • PPAR alpha
  • SLC2A1 protein, human
  • Glucose