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The role of Nanog expression in tamoxifen-resistant breast cancer cells
There is an accumulation of evidence that shows a significant role of cancer stem cells in tumor initiation, proliferation, relapse, and metastasis. Nanog is the most important core transcription marker of stem cells, known by its role in maintaining pluripotency, proliferation, and differentiation....
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4461083/ https://www.ncbi.nlm.nih.gov/pubmed/26082649 http://dx.doi.org/10.2147/OTT.S67835 |
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author | Arif, Khalid Hussain, Issam Rea, Carol El-Sheemy, Mohamed |
author_facet | Arif, Khalid Hussain, Issam Rea, Carol El-Sheemy, Mohamed |
author_sort | Arif, Khalid |
collection | PubMed |
description | There is an accumulation of evidence that shows a significant role of cancer stem cells in tumor initiation, proliferation, relapse, and metastasis. Nanog is the most important core transcription marker of stem cells, known by its role in maintaining pluripotency, proliferation, and differentiation. Therefore, this study aimed to examine the role of Nanog in breast cancer cell tamoxifen resistance and its implications in breast cancer treatment. In this study, the expression of the three core transcription markers Nanog, Oct3/4, and Sox2 were quantitatively evaluated using flow cytometry. Then, small interfering RNA (siRNA) against human Nanog was transfected into tamoxifen-resistant breast cancer cells via Lipofectamine 2000. Nanog gene expression in the cells was detected using reverse transcription polymerase chain reaction (RT-PCR). The change in cell proliferation was evaluated using the tetrazolium bromide method. An enzyme-linked immunosorbent assay was used to detect apoptosis of the transfected cells alone and in combination with 4-hydroxytamoxifen. The results showed a high level expression of Nanog, Oct3/4, and Sox2 in MDA-MB-231 and MCF7/tamoxifen resistant cells compared with MCF7/wild-type. siRNA-mediated Nanog gene silencing can efficiently inhibit cell proliferation and induce apoptosis of tamoxifen-resistant breast cancer cells. This study provides a basis for further study of the role of Nanog in developing resistance to tamoxifen, its implication in breast cancer management, and as a new strategy to enhance response to endocrine therapy. |
format | Online Article Text |
id | pubmed-4461083 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-44610832015-06-16 The role of Nanog expression in tamoxifen-resistant breast cancer cells Arif, Khalid Hussain, Issam Rea, Carol El-Sheemy, Mohamed Onco Targets Ther Original Research There is an accumulation of evidence that shows a significant role of cancer stem cells in tumor initiation, proliferation, relapse, and metastasis. Nanog is the most important core transcription marker of stem cells, known by its role in maintaining pluripotency, proliferation, and differentiation. Therefore, this study aimed to examine the role of Nanog in breast cancer cell tamoxifen resistance and its implications in breast cancer treatment. In this study, the expression of the three core transcription markers Nanog, Oct3/4, and Sox2 were quantitatively evaluated using flow cytometry. Then, small interfering RNA (siRNA) against human Nanog was transfected into tamoxifen-resistant breast cancer cells via Lipofectamine 2000. Nanog gene expression in the cells was detected using reverse transcription polymerase chain reaction (RT-PCR). The change in cell proliferation was evaluated using the tetrazolium bromide method. An enzyme-linked immunosorbent assay was used to detect apoptosis of the transfected cells alone and in combination with 4-hydroxytamoxifen. The results showed a high level expression of Nanog, Oct3/4, and Sox2 in MDA-MB-231 and MCF7/tamoxifen resistant cells compared with MCF7/wild-type. siRNA-mediated Nanog gene silencing can efficiently inhibit cell proliferation and induce apoptosis of tamoxifen-resistant breast cancer cells. This study provides a basis for further study of the role of Nanog in developing resistance to tamoxifen, its implication in breast cancer management, and as a new strategy to enhance response to endocrine therapy. Dove Medical Press 2015-06-03 /pmc/articles/PMC4461083/ /pubmed/26082649 http://dx.doi.org/10.2147/OTT.S67835 Text en © 2015 Arif et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Arif, Khalid Hussain, Issam Rea, Carol El-Sheemy, Mohamed The role of Nanog expression in tamoxifen-resistant breast cancer cells |
title | The role of Nanog expression in tamoxifen-resistant breast cancer cells |
title_full | The role of Nanog expression in tamoxifen-resistant breast cancer cells |
title_fullStr | The role of Nanog expression in tamoxifen-resistant breast cancer cells |
title_full_unstemmed | The role of Nanog expression in tamoxifen-resistant breast cancer cells |
title_short | The role of Nanog expression in tamoxifen-resistant breast cancer cells |
title_sort | role of nanog expression in tamoxifen-resistant breast cancer cells |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4461083/ https://www.ncbi.nlm.nih.gov/pubmed/26082649 http://dx.doi.org/10.2147/OTT.S67835 |
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