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Epidermal growth factor suppresses induction by progestin of the adhesion protein desmoplakin in T47D breast cancer cells
INTRODUCTION: Although the effects of progesterone on cell cycle progression are well known, its role in spreading and adhesion of breast cancer cells has not attracted much attention until recently. Indeed, by controlling cell adhesion proteins, progesterone may play a direct role in breast cancer...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2004
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC400677/ https://www.ncbi.nlm.nih.gov/pubmed/15084247 http://dx.doi.org/10.1186/bcr780 |
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author | Pang, Haiyan Rowan, Brian G Al-Dhaheri, Mariam Faber, Lee E |
author_facet | Pang, Haiyan Rowan, Brian G Al-Dhaheri, Mariam Faber, Lee E |
author_sort | Pang, Haiyan |
collection | PubMed |
description | INTRODUCTION: Although the effects of progesterone on cell cycle progression are well known, its role in spreading and adhesion of breast cancer cells has not attracted much attention until recently. Indeed, by controlling cell adhesion proteins, progesterone may play a direct role in breast cancer invasion and metastasis. Progesterone has also been shown to modulate epidermal growth factor (EGF) effects in neoplasia, although EGF effects on progesterone pathways and targets are less well understood. In the present study we identify an effect of EGF on a progesterone target, namely desmoplakin. METHODS: Initially flow cytometry was used to establish the growing conditions and demonstrate that the T47D breast cancer cell line was responding to progesterone and EGF in a classical manner. Differential display RT-PCR was employed to identify differentially expressed genes affected by progesterone and EGF. Western and Northern blotting were used to verify interactions between EGF and progesterone in three breast cancer cell lines: T47D, MCF-7, and ZR-75. RESULTS: We found the cell adhesion protein desmoplakin to be upregulated by progesterone – a process that was suppressed by EGF. This appears to be a general but not universal effect in breast cancer cell lines. CONCLUSION: Our findings suggest that progesterone and EGF may play opposing roles in metastasis. They also suggest that desmoplakin may be a useful biomarker for mechanistic studies designed to analyze the crosstalk between EGF and progesterone dependent events. Our work may help to bridge the fields of metastasis and differentiation, and the mechanisms of steroid action. |
format | Text |
id | pubmed-400677 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2004 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-4006772004-05-01 Epidermal growth factor suppresses induction by progestin of the adhesion protein desmoplakin in T47D breast cancer cells Pang, Haiyan Rowan, Brian G Al-Dhaheri, Mariam Faber, Lee E Breast Cancer Res Research Article INTRODUCTION: Although the effects of progesterone on cell cycle progression are well known, its role in spreading and adhesion of breast cancer cells has not attracted much attention until recently. Indeed, by controlling cell adhesion proteins, progesterone may play a direct role in breast cancer invasion and metastasis. Progesterone has also been shown to modulate epidermal growth factor (EGF) effects in neoplasia, although EGF effects on progesterone pathways and targets are less well understood. In the present study we identify an effect of EGF on a progesterone target, namely desmoplakin. METHODS: Initially flow cytometry was used to establish the growing conditions and demonstrate that the T47D breast cancer cell line was responding to progesterone and EGF in a classical manner. Differential display RT-PCR was employed to identify differentially expressed genes affected by progesterone and EGF. Western and Northern blotting were used to verify interactions between EGF and progesterone in three breast cancer cell lines: T47D, MCF-7, and ZR-75. RESULTS: We found the cell adhesion protein desmoplakin to be upregulated by progesterone – a process that was suppressed by EGF. This appears to be a general but not universal effect in breast cancer cell lines. CONCLUSION: Our findings suggest that progesterone and EGF may play opposing roles in metastasis. They also suggest that desmoplakin may be a useful biomarker for mechanistic studies designed to analyze the crosstalk between EGF and progesterone dependent events. Our work may help to bridge the fields of metastasis and differentiation, and the mechanisms of steroid action. BioMed Central 2004 2004-03-18 /pmc/articles/PMC400677/ /pubmed/15084247 http://dx.doi.org/10.1186/bcr780 Text en Copyright © 2004 Pang et al., licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL. |
spellingShingle | Research Article Pang, Haiyan Rowan, Brian G Al-Dhaheri, Mariam Faber, Lee E Epidermal growth factor suppresses induction by progestin of the adhesion protein desmoplakin in T47D breast cancer cells |
title | Epidermal growth factor suppresses induction by progestin of the adhesion protein desmoplakin in T47D breast cancer cells |
title_full | Epidermal growth factor suppresses induction by progestin of the adhesion protein desmoplakin in T47D breast cancer cells |
title_fullStr | Epidermal growth factor suppresses induction by progestin of the adhesion protein desmoplakin in T47D breast cancer cells |
title_full_unstemmed | Epidermal growth factor suppresses induction by progestin of the adhesion protein desmoplakin in T47D breast cancer cells |
title_short | Epidermal growth factor suppresses induction by progestin of the adhesion protein desmoplakin in T47D breast cancer cells |
title_sort | epidermal growth factor suppresses induction by progestin of the adhesion protein desmoplakin in t47d breast cancer cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC400677/ https://www.ncbi.nlm.nih.gov/pubmed/15084247 http://dx.doi.org/10.1186/bcr780 |
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