Epigallocatechin-3-gallate promotes apoptosis in human breast cancer T47D cells through down-regulation of PI3K/AKT and Telomerase
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. IC 50 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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EGCG induces apoptosis in Hep-2 cells in a dose-dependent manner through inhibition of telomerase.
“EGCG was shown to induce apoptosis in Hep-2 cells in a dose-dependent manner through the inhibition of telomerase.”
From Drug repurposing for cancer therapy (2024) · cites this paper as [146]
EGCG induces apoptosis in T47D breast cancer cells via inhibition of telomerase and PI3K/AKT pathways and simultaneous upregulation of P53 and Bax/Bcl-2 pathways.
“EGCG was found to induce apoptosis in T47D breast cancer cells via inhibition of the telomerase and PI3K/AKT pathways and simultaneous upregulation of the P53 and Bax/Bcl-2 pathways.”
From Drug repurposing for cancer therapy (2024) · cites this paper as [146]
EGCG induces apoptosis in cancer cells without manifesting notable toxicity to healthy cells.
“EGCG was able to induce apoptosis in cancer cells without manifesting notable toxicity to healthy cells.146”
From Drug repurposing for cancer therapy (2024) · cites this paper as [146]
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- Authors
- Moradzadeh, M., Hosseini, A., Erfanian, S., & Rezaei, H.
- Affiliations
- Mashhad University of Medical Sciences (IR)
- Jahrom University of Medical Sciences (IR)
- Corresponding author
- Erfanian, Saiedeh
- Venue
- Pharmacological Reports
- Published
- 2017-10
- Volume
- 69
- Issue
- 5
- Pages
- 924-928
- ISSN
- 1734-1140 (ISSN-L)
- OpenAlex
- W2605916518
- Cited by
- 127
- References
- 33
- Citations by year
- 2026: 9 · 2025: 13 · 2024: 16 · 2023: 13 · 2022: 17 · 2021: 17 · 2020: 15 · 2019: 9 · 2018: 11 · 2017: 7
- FWCI
- 9.05
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Pharmacological Reports (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Tea Polyphenols and Effects
- Health Sciences › Medicine › Pharmacology › Flavonoids in Medical Research
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Natural Compound Pharmacology Studies
- Keywords
- epigallocatechin gallate, green tea, breast cancer, T47D cells, apoptosis, PI3K/Akt signaling, telomerase, hTERT, estrogen receptor alpha, tamoxifen, Bax/Bcl-2 ratio, caspase-3, caspase-9, PTEN, cell proliferation
- MeSH terms
- Antioxidants, Breast Neoplasms, Catechin, Cell Survival, Female, Humans, Down-Regulation, Gene Expression Regulation, Neoplastic, Apoptosis, Telomerase, Phosphatidylinositol 3-Kinases, Cell Line, Tumor, Proto-Oncogene Proteins c-akt
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