Format

Send to

Choose Destination
Molecules. 2016 Dec 9;21(12). pii: E1679.

Cancer Preventive Activities of Tea Catechins.

Author information

1
Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ 08854-8020, USA. csyang@pharmacy.rutgers.edu.
2
Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ 08854-8020, USA. howang@rci.rutgers.edu.

Abstract

Catechins are widely occurring in our diet and beverages. The cancer-preventive activities of catechins have been extensively studied. Of these, (-)-epigallocatechin-3-gallate (EGCG), the principal catechin in green tea, has received the most attention. The inhibitory activities of tea catechins against carcinogenesis and cancer cell growth have been demonstrated in a large number of laboratory studies. Many mechanisms for modulating cancer signaling and metabolic pathways have been proposed based on numerous studies in cell lines with EGCG, the most active tea catechin. Nevertheless, it is not known whether many of these mechanisms indeed contribute to the anti-cancer activities in animals and in humans. Human studies have provided some results for the cancer preventive activities of tea catechins; however, the activities are not strong. This article reviews the cancer preventive activities and mechanisms of action of tea catechins involving their redox activities, biochemical properties and binding to key enzymes or signal transduction proteins. These mechanisms lead to suppression of cell proliferation, increased apoptosis and inhibition of angiogenesis. The relevance of the proposed mechanisms for cancer prevention are assessed in the light of the situation in vivo. The potential and possible problems in the application of tea and tea-derived products for cancer prevention are discussed.

KEYWORDS:

EGCG; animal models; cancer signaling; cell lines; tea catechins

PMID:
27941682
PMCID:
PMC6273642
DOI:
10.3390/molecules21121679
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Multidisciplinary Digital Publishing Institute (MDPI) Icon for PubMed Central
Loading ...
Support Center