Early transcriptional pattern of angiogenesis induced by EGCG treatment in cervical tumour cells

J Cell Mol Med. 2012 Mar;16(3):520-30. doi: 10.1111/j.1582-4934.2011.01346.x.

Abstract

The major green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) has been shown to exhibit antitumour activities in several tumour models. One of the possible mechanisms by which EGCG can inhibit cancer progression is through the modulation of angiogenesis signalling cascade. The tumour cells' ability to tightly adhere to endothelium is a very important process in the metastatic process, because once disseminated into the bloodstream the tumour cells must re-establish adhesive connections to endothelium in order to extravasate into the target tissues. In this study, we investigated the anti-angiogenic effects of EGCG treatment (10 μM) on human cervical tumour cells (HeLa) by evaluating the changes in the expression pattern of 84 genes known to be involved in the angiogenesis process. Transcriptional analysis revealed 11 genes to be differentially expressed and was further validated by measuring the induced biological effects. Our results show that EGCG treatment not only leads to the down-regulation of genes involved in the stimulation of proliferation, adhesion and motility as well as invasion processes, but also to the up-regulation of several genes known to have antagonist effects. We observed reduced proliferation rates, adhesion and spreading ability as well as invasiveness of HeLa tumour cells upon treatment, which suggest that EGCG might be an important anti-angiogenic therapeutic approach in cervical cancers.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiogenesis Inhibitors / pharmacology*
  • Apoptosis / drug effects
  • Catechin / analogs & derivatives*
  • Catechin / pharmacology
  • Cell Adhesion / drug effects
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects
  • Collagen
  • Drug Combinations
  • Female
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic / drug effects*
  • HeLa Cells / drug effects
  • Human Umbilical Vein Endothelial Cells / drug effects
  • Humans
  • Laminin
  • Neoplasm Invasiveness / prevention & control
  • Neovascularization, Pathologic
  • Proteoglycans
  • Signal Transduction
  • Transcription, Genetic / drug effects
  • Uterine Cervical Neoplasms / blood supply
  • Uterine Cervical Neoplasms / drug therapy*
  • Uterine Cervical Neoplasms / genetics

Substances

  • Angiogenesis Inhibitors
  • Drug Combinations
  • Laminin
  • Proteoglycans
  • matrigel
  • Catechin
  • Collagen
  • epigallocatechin gallate