Antiproliferation effect of guanosine on HCT 116 cells involves MAPK and AMPK pathways

Nucleosides Nucleotides Nucleic Acids. 2017 Apr 3;36(4):243-255. doi: 10.1080/15257770.2016.1268693. Epub 2017 Mar 21.

Abstract

This study aims to investigate the mechanisms associated with the antiproliferation effect of guanosine on human colon carcinoma HCT 116 cells. In this study, guanosine induced more drastic cell cycle arrest effect than cell death effect on HCT 116 cells. The cell cycle arrest effect of guanosine on HCT 116 cells appeared to be associated with the increased activation of mitogen-activated protein kinases (MAPK) such as ERK1/2, p38 and JNK. The decrease of AMP-activated protein kinase (AMPK) activation and cyclin D1 expression was also involved. Thus, the antiproliferation of colon cancer cells of guanosine could be mediated by the disruption of MAPK and AMPK pathways.

Keywords: Guanosine; HCT 116 cells; cell cycle; cell signalling.

MeSH terms

  • AMP-Activated Protein Kinases / metabolism*
  • Antineoplastic Agents / pharmacology*
  • Cell Cycle Checkpoints / drug effects
  • Cell Proliferation / drug effects
  • Cyclin D1 / metabolism
  • Enzyme Activation / drug effects
  • Guanosine / pharmacology*
  • HCT116 Cells
  • Humans
  • MAP Kinase Signaling System / drug effects
  • Mitogen-Activated Protein Kinases / metabolism*
  • Mitogen-Activated Protein Kinases / pharmacokinetics
  • Phosphorylation / drug effects

Substances

  • Antineoplastic Agents
  • Guanosine
  • Cyclin D1
  • Mitogen-Activated Protein Kinases
  • AMP-Activated Protein Kinases