Curcumin induces FasL-related apoptosis through p38 activation in human hepatocellular carcinoma Huh7 cells

Life Sci. 2013 Mar 14;92(6-7):352-8. doi: 10.1016/j.lfs.2013.01.013. Epub 2013 Jan 24.

Abstract

Aim: The aim of this study is to explore the underlying molecular mechanism of curcumin-induced apoptosis in human hepatocellular carcinoma (HCC) Huh7 cells.

Main methods: Fas and FasL mRNA expression was analyzed by reverse transcription PCR. Western blot was applied to detect the protein expression of Bcl-2 family members, MAPK family members, c-Jun, c-Fos, ATF-2, caspase-3, PARP, TNF receptor family members and the respective ligands. Apoptotic cells were assayed with annexin V/PI double staining and flow cytometry.

Key findings: Curcumin treatment resulted in a fast and significant increase of Fas and Fas ligand (FasL) along with activation of caspase-3 and cleavage of PARP in Huh7 cells. Inhibition of caspase-3 activity by the specific inhibitor Z-DEVD-FMK rescued Huh7 cells from curcumin-induced apoptosis. Neutralization of FasL significantly protected the cells from curcumin-induced caspase-3 activation and apoptosis in a dose-dependent manner. Moreover, p38 was rapidly activated in response to curcumin, and inactivation of p38 by pharmacologic inhibitor SB203580 dramatically suppressed curcumin-induced FasL expression and apoptosis.

Significance: Our results demonstrated that curcumin induces apoptosis through p38-denpendent up-regulation of FasL in Huh7 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Carcinoma, Hepatocellular / pathology
  • Caspase 3 / biosynthesis
  • Caspase Inhibitors / pharmacology
  • Cell Line, Tumor
  • Curcumin / pharmacology*
  • Fas Ligand Protein / biosynthesis*
  • Humans
  • Imidazoles / pharmacology
  • Oligopeptides / pharmacology
  • Phosphorylation / drug effects
  • Pyridines / pharmacology
  • Signal Transduction / drug effects
  • Up-Regulation / drug effects
  • fas Receptor / biosynthesis*
  • p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • p38 Mitogen-Activated Protein Kinases / metabolism*

Substances

  • Caspase Inhibitors
  • FAS protein, human
  • FASLG protein, human
  • Fas Ligand Protein
  • Imidazoles
  • Oligopeptides
  • Pyridines
  • benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone
  • fas Receptor
  • p38 Mitogen-Activated Protein Kinases
  • Caspase 3
  • Curcumin
  • SB 203580