Catechin hydrate suppresses MCF-7 proliferation through TP53/Caspase-mediated apoptosis

J Exp Clin Cancer Res. 2010 Dec 17;29(1):167. doi: 10.1186/1756-9966-29-167.

Abstract

Catechin hydrate (CH), a strong antioxidant that scavenges radicals, is a phenolic compound that is extracted from plants and is present in natural food and drinks, such as green tea and red wine. CH possesses anticancer potential. The mechanism of action of many anticancer drugs is based on their ability to induce apoptosis. In this study, I sought to characterize the downstream apoptotic genes targeted by CH in MCF-7 human breast cancer cells. CH effectively kills MCF-7 cells through induction of apoptosis. Apoptosis was confirmed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and real-time PCR assays. Cells were exposed to 150 μg/ml CH and 300 μg/mL CH for 24 hours, which resulted in 40.7% and 41.16% apoptotic cells, respectively. Moreover, a 48-hour exposure to 150 μg/ml CH and 300 μg/ml CH resulted in 43.73% and 52.95% apoptotic cells, respectively. Interestingly, after 72 hours of exposure to both concentrations of CH, almost 100% of cells lost their integrity. These results were further confirmed by the increased expression of caspase-3,-8, and -9 and TP53 in a time-dependent and dose-dependent manner, as determined by real-time quantitative PCR. In summary, the induction of apoptosis by CH is affected by its ability to increase the expression of pro-apoptotic genes such as caspase-3, -8, and -9 and TP53.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Antioxidants / pharmacology
  • Apoptosis / drug effects*
  • Breast Neoplasms / metabolism*
  • Caspases / drug effects
  • Caspases / metabolism
  • Catechin / pharmacology*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Female
  • Humans
  • In Situ Nick-End Labeling
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction / drug effects
  • Tumor Suppressor Protein p53 / drug effects
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Antineoplastic Agents
  • Antioxidants
  • Tumor Suppressor Protein p53
  • Catechin
  • Caspases