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Mechanism of EGCG promoting apoptosis of MCF-7 cell line in human breast cancer
The aim of the present study was to investigate the effects of epigallocatechin-3-gallate (EGCG) on the apoptosis of the human MCF-7 cancer cell line and the underlying mechanism. MCF-7 cells were divided into the control group and EGCG groups. The proliferation of MCF-7 cells in the two groups was...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5588052/ https://www.ncbi.nlm.nih.gov/pubmed/28927122 http://dx.doi.org/10.3892/ol.2017.6641 |
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author | Huang, Chao-You Han, Zheng Li, Xi Xie, Hui-Hua Zhu, Shan-Shan |
author_facet | Huang, Chao-You Han, Zheng Li, Xi Xie, Hui-Hua Zhu, Shan-Shan |
author_sort | Huang, Chao-You |
collection | PubMed |
description | The aim of the present study was to investigate the effects of epigallocatechin-3-gallate (EGCG) on the apoptosis of the human MCF-7 cancer cell line and the underlying mechanism. MCF-7 cells were divided into the control group and EGCG groups. The proliferation of MCF-7 cells in the two groups was determined using MTT and apoptosis was examined using flow cytometry. Western blot analysis and qRT-PCR were used to analyze P53 and Bcl-2 expression levels. The silencing effect of specific siRNA was evaluated using RT-PCR and western blot analysis. P53 and Bcl-2 expression levels were determined using western blot analysis in the si-P53, EGCG and EGCG-combined si-P53 groups. EGCG inhibited the proliferation of MCF-7 cells in a concentration-dependent manner and IC(50) was 37.681 mol/l. The apoptotic rates were 1.37 and 5.83% (t=8.9, p=0.0124) in the blank control and treatment groups after treatment with 30 µmol/l EGCG. The RT-qPCR and western blot results demonstrated that the effect of siRNA interference was evident. The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group. The Bcl-2 expression level in the EGCG-combined si-P53 group was lower than that of the si-P53 group and higher than that of the EGCG group. In conclusion, EGCG suppressed the proliferation of human MCF-7 breast cancer cells and promoted apoptosis. In addition, the underlying mechanism may be related to the P53/Bcl-2 signaling pathway. |
format | Online Article Text |
id | pubmed-5588052 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-55880522017-09-18 Mechanism of EGCG promoting apoptosis of MCF-7 cell line in human breast cancer Huang, Chao-You Han, Zheng Li, Xi Xie, Hui-Hua Zhu, Shan-Shan Oncol Lett Articles The aim of the present study was to investigate the effects of epigallocatechin-3-gallate (EGCG) on the apoptosis of the human MCF-7 cancer cell line and the underlying mechanism. MCF-7 cells were divided into the control group and EGCG groups. The proliferation of MCF-7 cells in the two groups was determined using MTT and apoptosis was examined using flow cytometry. Western blot analysis and qRT-PCR were used to analyze P53 and Bcl-2 expression levels. The silencing effect of specific siRNA was evaluated using RT-PCR and western blot analysis. P53 and Bcl-2 expression levels were determined using western blot analysis in the si-P53, EGCG and EGCG-combined si-P53 groups. EGCG inhibited the proliferation of MCF-7 cells in a concentration-dependent manner and IC(50) was 37.681 mol/l. The apoptotic rates were 1.37 and 5.83% (t=8.9, p=0.0124) in the blank control and treatment groups after treatment with 30 µmol/l EGCG. The RT-qPCR and western blot results demonstrated that the effect of siRNA interference was evident. The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group. The Bcl-2 expression level in the EGCG-combined si-P53 group was lower than that of the si-P53 group and higher than that of the EGCG group. In conclusion, EGCG suppressed the proliferation of human MCF-7 breast cancer cells and promoted apoptosis. In addition, the underlying mechanism may be related to the P53/Bcl-2 signaling pathway. D.A. Spandidos 2017-09 2017-07-20 /pmc/articles/PMC5588052/ /pubmed/28927122 http://dx.doi.org/10.3892/ol.2017.6641 Text en Copyright: © Huang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Huang, Chao-You Han, Zheng Li, Xi Xie, Hui-Hua Zhu, Shan-Shan Mechanism of EGCG promoting apoptosis of MCF-7 cell line in human breast cancer |
title | Mechanism of EGCG promoting apoptosis of MCF-7 cell line in human breast cancer |
title_full | Mechanism of EGCG promoting apoptosis of MCF-7 cell line in human breast cancer |
title_fullStr | Mechanism of EGCG promoting apoptosis of MCF-7 cell line in human breast cancer |
title_full_unstemmed | Mechanism of EGCG promoting apoptosis of MCF-7 cell line in human breast cancer |
title_short | Mechanism of EGCG promoting apoptosis of MCF-7 cell line in human breast cancer |
title_sort | mechanism of egcg promoting apoptosis of mcf-7 cell line in human breast cancer |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5588052/ https://www.ncbi.nlm.nih.gov/pubmed/28927122 http://dx.doi.org/10.3892/ol.2017.6641 |
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