Artemisinin inhibits neuroblastoma proliferation through activation of AHP-activated protein kinase (AMPK) signaling

Pharmazie. 2014 Jun;69(6):468-72.

Abstract

Recent population studies suggest that the use of artemisinin is associated with reduced incidence and improved prognosis of certain cancers. In the current study, we assessed the effect of artemisinin on neuroblastoma cells using SHSY5Y cells. We found that artemisinin inhibited growth and modulated expression of cell-cycle regulators in these cells. Treatment with artemisinin was also associated with activation of AMP kinase and inhibition of mTOR/p70S6K/pS6 signaling in SHSY5Y cells. In addition, inhibition of AMPK signaling reversed impact on the anti-proliferative roles of artemisinin. Taken together, these results provide evidence for a mechanism that may contribute to the antineoplastic effects of artemisinin suggested by recent population studies and justify further work to explore its potential roles in neuroblastoma prevention and treatment.

MeSH terms

  • Animals
  • Antimalarials / pharmacology*
  • Antimetabolites
  • Antineoplastic Agents*
  • Artemisinins / pharmacology*
  • Blotting, Western
  • Brain Neoplasms / drug therapy*
  • Bromodeoxyuridine
  • Cell Cycle Proteins / biosynthesis
  • Cell Cycle Proteins / genetics
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors*
  • Dose-Response Relationship, Drug
  • Humans
  • Neuroblastoma / drug therapy*
  • RNA / biosynthesis
  • RNA / isolation & purification
  • RNA, Small Interfering / genetics
  • Real-Time Polymerase Chain Reaction

Substances

  • Antimalarials
  • Antimetabolites
  • Antineoplastic Agents
  • Artemisinins
  • Cell Cycle Proteins
  • RNA, Small Interfering
  • RNA
  • artemisinin
  • Cyclic AMP-Dependent Protein Kinases
  • Bromodeoxyuridine