Flavonoids (apigenin, tangeretin) counteract tumor promoter-induced inhibition of intercellular communication of rat liver epithelial cells

Cancer Lett. 1997 Mar 19;114(1-2):207-10. doi: 10.1016/s0304-3835(97)04664-8.

Abstract

We have shown previously that two flavonoids, apigenin and tangeretin, enhance gap junctional intercellular communication (GJIC) in rat liver epithelial cells, named REL cells. Here, we show that these two flavones also antagonize the inhibition of GJIC induced by tumor promoters like 12-O-tetradecanoyl-phorbol-acetate (TPA) and 3,5,di-tertio-butyl-4-hydroxytoluene (BHT). Their preventive effect is rapid. It does not seem to involve any change of the amount of the connexin expressed in REL cells, connexin 43 (Cx 43), and in its phosphorylation state. Other flavonoids tested including naringenin, myricetin, catechin and chrysin did not enhance GJIC nor counteract TPA-induced inhibition of GJIC.

MeSH terms

  • Animals
  • Blotting, Western
  • Butylated Hydroxytoluene / pharmacology
  • Carcinogens / antagonists & inhibitors*
  • Cells, Cultured
  • Chamomile
  • Connexin 43 / metabolism
  • Dimethyl Sulfoxide / pharmacology
  • Epithelium / drug effects
  • Flavones*
  • Flavonoids / pharmacology*
  • Fluorescent Antibody Technique
  • Gap Junctions / drug effects
  • Liver / drug effects*
  • Oils, Volatile / pharmacology*
  • Phosphorylation / drug effects
  • Plants, Medicinal
  • Rats
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Carcinogens
  • Connexin 43
  • Flavones
  • Flavonoids
  • Oils, Volatile
  • Butylated Hydroxytoluene
  • tangeretin
  • Tetradecanoylphorbol Acetate
  • Dimethyl Sulfoxide