Background: Breast cancer is the most frequent cancer in women. Green tea has been studied for breast cancer chemopreventive and possibly chemotherapeutic effects due to its high content in polyphenolic compounds, including epigallocatechin-3-gallate (EGCG). Method: This review is based on a literature research that included papers registered on the Medline database. The research was conducted through PubMed, with the application of the following query: “EGCG”AND "breast cancer”. The result was a total of 88 articles in which this review stands on. Results: In vitro, EGCG shows antioxidant or pro-oxidant properties, depending on the concentration and exposure time. EGCG blocks cell cycle progression and modulates signaling pathways that affects cell proliferation and differentiation. EGCG also induces apoptosis, negatively modulates different steps involved in metastasis and targets angiogenesis by inhibiting VEGF transcription. In vivo, investigations have shown that oral administration of EGCG results in reduction of tumor growth and in antimetastatic and antiangiogenic effects in animal xenograft and allograft models. Discussion: Much remains unknown about the molecular mechanisms involved in the protective effects of EGCG on mammary carcinogenesis. In addition, more studies in vivo are necessary to determine the potential toxicity of EGCG at higher doses and to elucidate its interactions with other drugs. Conclusion: A protective effect of EGCG has been shown in different experimental models and under different experimental conditions, suggesting clinical implications of EGCG for breast cancer prevention and therapy. The data presented in this review support the importance of further investigations.

The murine breast cancer cells (4T1) grown both in female BALB/c mice and in culture were treated with anastrozole (50 µg/mL), tamoxifen citrate (5 µg/mL), and the combination of the two drugs in order to determine treatment efficacies, toxic potential, and the mechanism of cell death. The in vivo treatments were evaluated by monitoring tumor growth, development, and life span. The in vitro effects were measured through cell growth kinetics, cell proliferation, mitochondrial membrane potential disruption assay, and light and scanning electron microscopy. All drug treatments extended the mean life span of the 4T1-inoculated tumorbearing mice; however, only tamoxifen and combination treatments statistically increased the life span when compared to untreated mice. Although the most drug inhibitory effect on cell multiplication was observed in the combination treatment, both anastrozole and tamoxifen individually inhibited cell proliferation significantly at most time periods in this mouse breast cancer cell line. The mitochondrial membrane potential disruption assay demonstrated significant increase in the percent of cells undergoing apoptosis in all treatment groups. However, the combination treatment was the most effective in inducing cell death via apoptosis. Light and scanning electron microscopy of the treated cells revealed characteristics such as rounding, clumping, and shrinkage of the cells as well as formation of cell surface blebbing and apoptotic bodies suggestive of cell death via apoptotic pathway.