4.4 Article

Epigallocatechin-3-gallate promotes apoptosis in human breast cancer T47D cells through down-regulation of PI3K/AKT and Telomerase

Journal

PHARMACOLOGICAL REPORTS
Volume 69, Issue 5, Pages 924-928

Publisher

POLISH ACAD SCIENCES INST PHARMACOLOGY
DOI: 10.1016/j.pharep.2017.04.008

Keywords

Breast cancer; Epigallocatechin-3-gallate; Telomerase; Apoptosis; PI3K/AKT signaling cascade

Funding

  1. Jahrom University of Medical Sciences, Jahrom, Iran

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Background: Green tea has antioxidant, anti-tumor and anti-bacterial properties. Epigallocatechin-3-gallate (EGCG) in green tea is highly active as a cancer chemopreventive agent. In this study, we designed a series of experiments to examine the effects of EGCG on proliferation and apoptosis of estrogen receptor a-positive breast cancer (T47D) cells. Methods: Cells were treated with EGCG (0-80 mu M) and tamoxifen (0-20 mu M), as the positive control, up to 72 h. Cell viability was determined by MTT assay. Apoptosis investigated by real time PCR of apoptosis and survival (Bax, Bcl-2, p21, p53, PTEN, PI3 K, AKT, caspase3 and caspase9 and hTERT) genes and by western blot of Bax/Bcl-2 proteins expressions. Results: The results showed that EGCG decreased cell viability as concentration-and time-dependently. IC50 values were 14.17 mu M for T47D and 193.10 mM for HFF cells, as compared with 3.39 mu M and 32.75 mu M for tamoxifen after 72 h treatment, respectively. Also, EGCG (80 mM) significantly increased the genes of PTEN, CASP3, CASP9 and decreased AKT approximately equal to tamoxifen. In gene expression, EGCG (80 mM) significantly increased Bax/Bcl-2 ratio to 8-fold vise 15-fold in tamoxifen (20 mu M)-treated T47D cells during 72 h. In protein expression of Bax/Bcl-2, EGCG significantly increased 6-fold while this ratio augmented 10-fold in tamoxifen group. EGCG significantly decreased 0.8, 0.4 and 0.3 gene expression of hTERT in 24, 48 and 72 h, respectively. Conclusions: This study suggests that EGCG may be a useful adjuvant therapeutic agent for the treatment of breast cancer. (c) 2017 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier Sp. z o.o. All rights reserved.

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