Molecular mechanisms of luteolin-7-O-glucoside-induced growth inhibition on human liver cancer cells: G2/M cell cycle arrest and caspase-independent apoptotic signaling pathways

BMB Rep. 2013 Dec;46(12):611-6. doi: 10.5483/bmbrep.2013.46.12.133.

Abstract

Luteolin-7-O-glucoside (LUT7G), a flavone subclass of flavonoids, has been found to increase anti-oxidant and anti-inflammatory activity, as well as cytotoxic effects. However, the mechanism of how LUT7G induces apoptosis and regulates cell cycles remains poorly understood. In this study, we examined the effects of LUT7G on the growth inhibition of tumors, cell cycle arrest, induction of ROS generation, and the involved signaling pathway in human hepatocarcinoma HepG2 cells. The proliferation of HepG2 cells was decreased by LUT7G in a dose-dependent manner. The growth inhibition was due primarily to the G2/M phase arrest and ROS generation. Moreover, the phosphorylation of JNK was increased by LUT7G. These results suggest that the anti-proliferative effect of LUT7G on HepG2 is associated with G2/M phase cell cycle arrest by JNK activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents, Phytogenic / pharmacology
  • Apoptosis / drug effects*
  • Caspases / metabolism*
  • Cell Proliferation / drug effects
  • Flavones / pharmacology*
  • G2 Phase Cell Cycle Checkpoints / drug effects*
  • Glucosides / pharmacology*
  • Hep G2 Cells
  • Humans
  • JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • Liver Neoplasms / metabolism
  • Liver Neoplasms / pathology
  • M Phase Cell Cycle Checkpoints / drug effects
  • Phosphorylation / drug effects
  • Reactive Oxygen Species / metabolism
  • Signal Transduction / drug effects*

Substances

  • Antineoplastic Agents, Phytogenic
  • Flavones
  • Glucosides
  • Reactive Oxygen Species
  • luteolin-7-glucoside
  • JNK Mitogen-Activated Protein Kinases
  • Caspases