Abstract

Tea leaf (Camellia sinensis) is rich in catechins, which endow tea with various health benefits. There are more than ten catechin compounds in tea, among which epigallocatechingallate (EGCG) is the most abundant. Epidemiological studies on the association between tea consumption and the risk of breast cancer were summarized, and the inhibitory effects of tea catechins on breast cancer, with EGCG as a representative compound, were reviewed in the present paper. The controversial results regarding the role of tea in breast cancer and areas for further study were discussed.

Highlights

  • Breast cancer is a common cancer in women

  • EGCG interacts with target proteins via hydrogen bonding, during which the hydroxyl groups of EGCG serve as hydrogen bond donors

  • Catechins can modulate the secretion of urokinase plasminogen activator, which is closely related to proteolytic enzymes in breast cancer cells and inhibits their invasive behavior by suppressing the transcription factors AP-1 and NF-κB [71]

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Summary

Introduction

Breast cancer is a common cancer in women. There were an estimated 1.7 million new cases Green tea polyphenols (GTP) are considered to be a potential candidate for further development as a chemoprotective factor for the primary prevention of age-related eye diseases [8]. There have been epidemiological and in vitro studies regarding the association of tea consumption with depression among breast cancer survivors [9]. Drinking tea or green tea was not associated with overall breast cancer risk [10]. The effects of tea and its catechins on the prevention of breast cancer are still inconclusive and controversial [11,12]. The present review will highlight the recent advances in the effects of tea and its catechins on breast cancer, including epidemiological, in vivo, and in vitro studies. The controversial results from in vitro and in vivo studies, as well as directions for further study are discussed in the present paper

Epidemiological Evidence
Suppressing Carcinogen-Induced ROS Elevation and DNA Damage
Regulating Cell Signaling Pathways
Interacting with Target Proteins
Inhibiting DNA Methylation
Inhibiting Tumor Angiogenesis
Anti-Proliferation and Inducing Breast Cancer Cell Apoptosis
Anti-Metastasis of Breast Cancer Cells
Inconsistent Results
Further Study Suggestions
Conclusions
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