Maliheh Moradzadeh1, Azar Hosseini2, Saiedeh Erfanian3, Hadi Rezaei4. 1. Department of New Sciences and Technology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 2. Pharmacological Research Center of Medicinal Plants, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 3. Research center for non-Communicable Diseases, Jahrom University of Medical Sciences, Jahrom, Iran. Electronic address: erfanian_85@yahoo.com. 4. Department of Microbiology, Jahrom University of Medical Sciences, Jahrom, Iran.
Abstract
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 α-positive breast cancer (T47D) cells. METHODS: Cells were treated with EGCG (0-80μM) and tamoxifen (0-20μM), as the positive control, up to 72h. Cell viability was determined by MTT assay. Apoptosis investigated by real time PCR of apoptosis and survival (Bax, Bcl-2, p21, p53, PTEN, PI3K, 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 14.17μM for T47D and 193.10μM for HFF cells, as compared with 3.39μM and 32.75μM for tamoxifen after 72h treatment, respectively. Also, EGCG (80μM) significantly increased the genes of PTEN, CASP3, CASP9 and decreased AKT approximately equal to tamoxifen. In gene expression, EGCG (80μM) significantly increased Bax/Bcl-2 ratio to 8-fold vise 15-fold in tamoxifen (20μM)-treated T47D cells during 72h. 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 72h, respectively. CONCLUSIONS: This study suggests that EGCG may be a useful adjuvant therapeutic agent for the treatment of breast cancer.
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 α-positive breast cancer (T47D) cells. METHODS: Cells were treated with EGCG (0-80μM) and tamoxifen (0-20μM), as the positive control, up to 72h. Cell viability was determined by MTT assay. Apoptosis investigated by real time PCR of apoptosis and survival (Bax, Bcl-2, p21, p53, PTEN, PI3K, 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 14.17μM for T47D and 193.10μM for HFF cells, as compared with 3.39μM and 32.75μM for tamoxifen after 72h treatment, respectively. Also, EGCG (80μM) significantly increased the genes of PTEN, CASP3, CASP9 and decreased AKT approximately equal to tamoxifen. In gene expression, EGCG (80μM) significantly increased Bax/Bcl-2 ratio to 8-fold vise 15-fold in tamoxifen (20μM)-treated T47D cells during 72h. 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 72h, respectively. CONCLUSIONS: This study suggests that EGCG may be a useful adjuvant therapeutic agent for the treatment of breast cancer.
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