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Review
. 2023 Jun 27;24(13):10737.
doi: 10.3390/ijms241310737.

The Potential Role of Epigallocatechin-3-Gallate (EGCG) in Breast Cancer Treatment

Víctor Marín  1 , Viviana Burgos  2   3 , Rebeca Pérez  1 , Durvanei Augusto Maria  4 , Paulo Pardi  5 , Cristian Paz  1
Affiliations
Review

The Potential Role of Epigallocatechin-3-Gallate (EGCG) in Breast Cancer Treatment

Víctor Marín et al. Int J Mol Sci. .

Abstract

Breast cancer is one of the most diagnosed cancers worldwide, with an incidence of 47.8%. Its treatment includes surgery, radiotherapy, chemotherapy, and antibodies giving a mortality of 13.6%. Breast tumor development is driven by a variety of signaling pathways with high heterogeneity of surface receptors, which makes treatment difficult. Epigallocatechin-3-gallate (EGCG) is a natural polyphenol isolated as the main component in green tea; it has shown multiple beneficial effects in breast cancer, controlling proliferation, invasion, apoptosis, inflammation, and demethylation of DNA. These properties were proved in vitro and in vivo together with synergistic effects in combination with traditional chemotherapy, increasing the effectiveness of the treatment. This review focuses on the effects of EGCG on the functional capabilities acquired by breast tumor cells during its multistep development, the molecular and signal pathways involved, the synergistic effects in combination with current drugs, and how nanomaterials can improve its bioavailability on breast cancer treatment.

Keywords: breast cancer; drug delivery; epigallocatechin-3-gallate; metabolism; synergistic chemotherapy.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Molecular structures of main catechins identified in green tea.
Figure 2
Figure 2
Multiple effects of EGCG in breast cancer. EGCG inhibits phosphorylation and activation of signaling pathways such as β-catenin, PI3K/AKT, and STAT3, preventing the translocation of its effectors to the nucleus. The main effect of this is the promotion of apoptosis and the inhibition of anti-apoptotic genes. In addition, this causes a decrease in the gene expression of the catalytic subunit of the telomerase enzyme hTERT. EGCG can act as a competitive inhibitor of hormones such as estradiol at key receptors for tumor growth, decrease its surface expression, alter its dispositions on the surface due to changes in lipid Rafts, or increase endosomal activity in the cell.
Figure 3
Figure 3
Metabolic pathways of EGCG by gut microbiota.
See this image and copyright information in PMC

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