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Cooperation between monocytes and breast cancer cells promotes factors involved in cancer aggressiveness
In breast cancers, clinical symptoms of inflammation localised around the tumour at the time of diagnosis have been considered to have poor prognosis significance. In this study, the biological mechanisms responsible for the deleterious action of monocytes in cancer were investigated. The incubation...
Autores principales: | , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2003
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747575/ https://www.ncbi.nlm.nih.gov/pubmed/12698185 http://dx.doi.org/10.1038/sj.bjc.6600872 |
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author | Blot, E Chen, W Vasse, M Paysant, J Denoyelle, C Pillé, J-Y Vincent, L Vannier, J-P Soria, J Soria, C |
author_facet | Blot, E Chen, W Vasse, M Paysant, J Denoyelle, C Pillé, J-Y Vincent, L Vannier, J-P Soria, J Soria, C |
author_sort | Blot, E |
collection | PubMed |
description | In breast cancers, clinical symptoms of inflammation localised around the tumour at the time of diagnosis have been considered to have poor prognosis significance. In this study, the biological mechanisms responsible for the deleterious action of monocytes in cancer were investigated. The incubation of the breast-cancer-derived MDA-MB231 cells with monocytes resulted in an increase in factors involved in cell invasion (i.e. both cancer cells and monocytes-associated urokinase and Tissue Factor, and PAI-1 and MMP-9 secretion). Moreover, the functions of monocytes were also modified. Incubation of monocytes with MDA-MB231 cancer cells resulted in a downregulation in the secretion of the antiproliferative cytokine Oncostatin M, while the apoptotic factor TNF alpha was dramatically increased. However, MDA-MB231 cancer cells have been shown to be resistant towards the apoptotic action of TNF alpha. These findings demonstrate that incubation of MDA-MB231 cancer cells with monocytes induced a crosstalk, which resulted in an increased expression of factors involved in cancer cell invasiveness and in a modification of monocytes function against cancer cells, while inflammatory effects were increased. |
format | Text |
id | pubmed-2747575 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2003 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-27475752009-09-21 Cooperation between monocytes and breast cancer cells promotes factors involved in cancer aggressiveness Blot, E Chen, W Vasse, M Paysant, J Denoyelle, C Pillé, J-Y Vincent, L Vannier, J-P Soria, J Soria, C Br J Cancer Molecular and Cellular Pathology In breast cancers, clinical symptoms of inflammation localised around the tumour at the time of diagnosis have been considered to have poor prognosis significance. In this study, the biological mechanisms responsible for the deleterious action of monocytes in cancer were investigated. The incubation of the breast-cancer-derived MDA-MB231 cells with monocytes resulted in an increase in factors involved in cell invasion (i.e. both cancer cells and monocytes-associated urokinase and Tissue Factor, and PAI-1 and MMP-9 secretion). Moreover, the functions of monocytes were also modified. Incubation of monocytes with MDA-MB231 cancer cells resulted in a downregulation in the secretion of the antiproliferative cytokine Oncostatin M, while the apoptotic factor TNF alpha was dramatically increased. However, MDA-MB231 cancer cells have been shown to be resistant towards the apoptotic action of TNF alpha. These findings demonstrate that incubation of MDA-MB231 cancer cells with monocytes induced a crosstalk, which resulted in an increased expression of factors involved in cancer cell invasiveness and in a modification of monocytes function against cancer cells, while inflammatory effects were increased. Nature Publishing Group 2003-04-22 2003-04-15 /pmc/articles/PMC2747575/ /pubmed/12698185 http://dx.doi.org/10.1038/sj.bjc.6600872 Text en Copyright © 2003 Cancer Research UK 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 | Molecular and Cellular Pathology Blot, E Chen, W Vasse, M Paysant, J Denoyelle, C Pillé, J-Y Vincent, L Vannier, J-P Soria, J Soria, C Cooperation between monocytes and breast cancer cells promotes factors involved in cancer aggressiveness |
title | Cooperation between monocytes and breast cancer cells promotes factors involved in cancer aggressiveness |
title_full | Cooperation between monocytes and breast cancer cells promotes factors involved in cancer aggressiveness |
title_fullStr | Cooperation between monocytes and breast cancer cells promotes factors involved in cancer aggressiveness |
title_full_unstemmed | Cooperation between monocytes and breast cancer cells promotes factors involved in cancer aggressiveness |
title_short | Cooperation between monocytes and breast cancer cells promotes factors involved in cancer aggressiveness |
title_sort | cooperation between monocytes and breast cancer cells promotes factors involved in cancer aggressiveness |
topic | Molecular and Cellular Pathology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747575/ https://www.ncbi.nlm.nih.gov/pubmed/12698185 http://dx.doi.org/10.1038/sj.bjc.6600872 |
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