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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...

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Autores principales: Huang, Chao-You, Han, Zheng, Li, Xi, Xie, Hui-Hua, Zhu, Shan-Shan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
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.
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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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