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Oestrogen and epidermal growth factor down-regulate erbB-2 oncogene protein expression in breast cancer cells by different mechanisms.
Mitogen-induced mammary cell growth is often accompanied by decreased levels of expression of the p185erbB-2 protein. We have previously reported that oestrogen inhibits erbB-2 mRNA and protein expression in breast cancer cells, while epidermal growth factor (EGF) treatment has been shown to decreas...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
1994
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033707/ https://www.ncbi.nlm.nih.gov/pubmed/7526884 |
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author | Antoniotti, S. Taverna, D. Maggiora, P. Sapei, M. L. Hynes, N. E. De Bortoli, M. |
author_facet | Antoniotti, S. Taverna, D. Maggiora, P. Sapei, M. L. Hynes, N. E. De Bortoli, M. |
author_sort | Antoniotti, S. |
collection | PubMed |
description | Mitogen-induced mammary cell growth is often accompanied by decreased levels of expression of the p185erbB-2 protein. We have previously reported that oestrogen inhibits erbB-2 mRNA and protein expression in breast cancer cells, while epidermal growth factor (EGF) treatment has been shown to decrease p185erbB-2 levels in normal mouse mammary epithelial cells. In the present work, we studied the effect of oestrogen and EGF on erbB-2 expression in oestrogen-responsive breast cancer cells. We observed that both oestrogen and EGF comparably down-regulated p185erbB-2 levels, while stimulating growth of T47D and ZR75.1 cells. Oestrogens, but not EGF, concomitantly down-regulated erbB-2 mRNA. Run-on analysis showed a reduced erbB-2 transcription rate in the presence of oestrogens. Furthermore, the transcriptional activity of a 219 bp proximal fragment of the human erbB-2 promoter was repressed by oestrogens, whereas it was enhanced by EGF. EGF stimulated both tyrosine phosphorylation and autokinase activity of p185erbB-2 down-regulates p185erbB-2 at a post-translational level. Thus, two factors converging in terms of effects on cell growth, display divergent mechanisms of regulation of erbB-2 expression. IMAGES: |
format | Text |
id | pubmed-2033707 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1994 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-20337072009-09-10 Oestrogen and epidermal growth factor down-regulate erbB-2 oncogene protein expression in breast cancer cells by different mechanisms. Antoniotti, S. Taverna, D. Maggiora, P. Sapei, M. L. Hynes, N. E. De Bortoli, M. Br J Cancer Research Article Mitogen-induced mammary cell growth is often accompanied by decreased levels of expression of the p185erbB-2 protein. We have previously reported that oestrogen inhibits erbB-2 mRNA and protein expression in breast cancer cells, while epidermal growth factor (EGF) treatment has been shown to decrease p185erbB-2 levels in normal mouse mammary epithelial cells. In the present work, we studied the effect of oestrogen and EGF on erbB-2 expression in oestrogen-responsive breast cancer cells. We observed that both oestrogen and EGF comparably down-regulated p185erbB-2 levels, while stimulating growth of T47D and ZR75.1 cells. Oestrogens, but not EGF, concomitantly down-regulated erbB-2 mRNA. Run-on analysis showed a reduced erbB-2 transcription rate in the presence of oestrogens. Furthermore, the transcriptional activity of a 219 bp proximal fragment of the human erbB-2 promoter was repressed by oestrogens, whereas it was enhanced by EGF. EGF stimulated both tyrosine phosphorylation and autokinase activity of p185erbB-2 down-regulates p185erbB-2 at a post-translational level. Thus, two factors converging in terms of effects on cell growth, display divergent mechanisms of regulation of erbB-2 expression. IMAGES: Nature Publishing Group 1994-12 /pmc/articles/PMC2033707/ /pubmed/7526884 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Research Article Antoniotti, S. Taverna, D. Maggiora, P. Sapei, M. L. Hynes, N. E. De Bortoli, M. Oestrogen and epidermal growth factor down-regulate erbB-2 oncogene protein expression in breast cancer cells by different mechanisms. |
title | Oestrogen and epidermal growth factor down-regulate erbB-2 oncogene protein expression in breast cancer cells by different mechanisms. |
title_full | Oestrogen and epidermal growth factor down-regulate erbB-2 oncogene protein expression in breast cancer cells by different mechanisms. |
title_fullStr | Oestrogen and epidermal growth factor down-regulate erbB-2 oncogene protein expression in breast cancer cells by different mechanisms. |
title_full_unstemmed | Oestrogen and epidermal growth factor down-regulate erbB-2 oncogene protein expression in breast cancer cells by different mechanisms. |
title_short | Oestrogen and epidermal growth factor down-regulate erbB-2 oncogene protein expression in breast cancer cells by different mechanisms. |
title_sort | oestrogen and epidermal growth factor down-regulate erbb-2 oncogene protein expression in breast cancer cells by different mechanisms. |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033707/ https://www.ncbi.nlm.nih.gov/pubmed/7526884 |
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