Phloretin induces cell cycle arrest and apoptosis of human glioblastoma cells through the generation of reactive oxygen species

J Neurooncol. 2016 Jun;128(2):217-23. doi: 10.1007/s11060-016-2107-z. Epub 2016 Mar 16.

Abstract

Phloretin, a flavonoid present in various plants, has been reported to exert anticarcinogenic effects. However, the mechanism of its chemo-preventive effect on human glioblastoma cells is not fully understood. This study aimed to investigate the molecular mechanism of phloretin and its associated chemo-preventive effect in human glioblastoma cells. The results indicate that phloretin inhibited cell proliferation by inducing cell cycle arrest at the G0-G1 phase and induced apoptosis of human glioblastoma cells. Phloretin-induced cell cycle arrest was associated with increased expression of p27 and decreased expression of cdk2, cdk4, cdk6, cyclinD and cyclinE. Moreover, the PI3K/AKT/mTOR signaling cascades were suppressed by phloretin in a dose-dependent manner. In addition, phloretin triggered the mitochondrial apoptosis pathway and generated reactive oxygen species (ROS). This was accompanied by the up-regulation of Bax, Bak and c-PARP and the down-regulation of Bcl-2. The antioxidant agents N-acetyl-L-cysteine and glutathione weakened the effect of phloretin on glioblastoma cells. In conclusion, these results demonstrate that phloretin exerts potent chemo-preventive activity in human glioblastoma cells through the generation of ROS.

Keywords: Apoptosis; Cell cycle arrest; Glioblastoma; Phloretin; Reactive oxygen species.

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Antioxidants / pharmacology
  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Caspase 9 / metabolism
  • Cell Cycle Checkpoints / drug effects*
  • Cell Cycle Checkpoints / physiology
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Proliferation / physiology
  • Glioblastoma / drug therapy*
  • Glioblastoma / metabolism
  • Humans
  • PTEN Phosphohydrolase / metabolism
  • Phloretin / pharmacology*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction / drug effects
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Antineoplastic Agents
  • Antioxidants
  • Reactive Oxygen Species
  • MTOR protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases
  • PTEN Phosphohydrolase
  • PTEN protein, human
  • CASP9 protein, human
  • Caspase 9
  • Phloretin