Apigenin induces apoptosis and impairs head and neck carcinomas EGFR/ErbB2 signaling

Front Biosci (Landmark Ed). 2011 Jan 1;16:1060-8. doi: 10.2741/3735.

Abstract

The development of head and neck squamous cell carcinomas (HNSCCs) is a multistep process progressing from precancerous lesions to highly malignant tumors. A critical role in HNSCCs development and progression is played by EGFR family members including EGFR and ErbB2. The aim of this study was to investigate the effect of apigenin, a low molecular weight flavonoid contained in fruits and vegetables, on growth and survival and on EGFR/ErbB2 signaling in cell lines derived from HNSCCs of the tongue (CAL-27, SCC-15) or pharynx (FaDu). Using sulforhodamine B assay, FACS analysis and activated caspase-3 detection by immunofluorescence, we here demonstrate that apigenin dose-dependently inhibits survival and induces apoptosis of HNSCC cells. Further, by performing western blotting with antibodies specific for phosphorylated EGFR, ErbB2, Erk1/2 and Akt we demonstrate that apigenin reduces ligand-induced phosphorylation of EGFR and ErbB2 and impairs their downstream signaling. On the whole, our results suggest that apigenin properties might be exploited for chemoprevention and/or therapy of head and neck carcinomas.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apigenin / pharmacology
  • Apigenin / therapeutic use*
  • Apoptosis / drug effects*
  • Carcinoma / drug therapy
  • Carcinoma, Squamous Cell
  • Cell Line, Tumor
  • ErbB Receptors / drug effects*
  • ErbB Receptors / physiology
  • Head and Neck Neoplasms / drug therapy
  • Humans
  • Neoplasms, Squamous Cell / drug therapy
  • Pharyngeal Neoplasms / drug therapy
  • Receptor, ErbB-2 / drug effects*
  • Receptor, ErbB-2 / physiology
  • Signal Transduction / drug effects
  • Squamous Cell Carcinoma of Head and Neck
  • Tongue Neoplasms / drug therapy

Substances

  • Apigenin
  • ErbB Receptors
  • Receptor, ErbB-2