Initiation of apoptosis, cell cycle arrest and autophagy of esophageal cancer cells by dihydroartemisinin

Biomed Pharmacother. 2013 Jun;67(5):417-24. doi: 10.1016/j.biopha.2013.01.013. Epub 2013 Feb 19.

Abstract

Dihydroartemisinin (DHA) has recently been shown anti-tumor activity in various cancer cells. However, its effect on esophageal cancer remains unclear. In this study, for the first time, we demonstrated that DHA reduced viability of esophageal cancer cells in a dose-dependent manner. The mechanism was at least partially due to DHA induced apoptosis by upregulating the expression of Bax, downregulating Bcl-2, Bcl-xL and Procaspase-3, and increasing caspase-9 activation, induced cell cycle arrest by downregulating cyclin E, CDK2 and CDK4. Furthermore, we firstly found that DHA induced autophagy in cancer cells. We concluded DHA might be a novel agent against esophageal cancer.

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects*
  • Artemisinins / administration & dosage
  • Artemisinins / pharmacology*
  • Autophagy / drug effects
  • Cell Cycle Checkpoints / drug effects
  • Cell Line, Tumor
  • Dose-Response Relationship, Drug
  • Down-Regulation / drug effects
  • Esophageal Neoplasms / drug therapy*
  • Esophageal Neoplasms / pathology
  • Humans
  • Up-Regulation / drug effects

Substances

  • Antineoplastic Agents
  • Artemisinins
  • artenimol