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SDF-1alpha concentration dependent modulation of RhoA and Rac1 modifies breast cancer and stromal cells interaction
BACKGROUND: The interaction of SDF-1alpha with its receptor CXCR4 plays a role in the occurrence of distant metastasis in many solid tumors. This interaction increases migration from primary sites as well as homing at distant sites. METHODS: Here we investigated how SDF-1α could modulate both migrat...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4522077/ https://www.ncbi.nlm.nih.gov/pubmed/26231656 http://dx.doi.org/10.1186/s12885-015-1556-7 |
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author | Pasquier, Jennifer Abu-Kaoud, Nadine Abdesselem, Houari Madani, Aisha Hoarau-Véchot, Jessica Thawadi, Hamda Al. Vidal, Fabien Couderc, Bettina Favre, Gilles Rafii, Arash |
author_facet | Pasquier, Jennifer Abu-Kaoud, Nadine Abdesselem, Houari Madani, Aisha Hoarau-Véchot, Jessica Thawadi, Hamda Al. Vidal, Fabien Couderc, Bettina Favre, Gilles Rafii, Arash |
author_sort | Pasquier, Jennifer |
collection | PubMed |
description | BACKGROUND: The interaction of SDF-1alpha with its receptor CXCR4 plays a role in the occurrence of distant metastasis in many solid tumors. This interaction increases migration from primary sites as well as homing at distant sites. METHODS: Here we investigated how SDF-1α could modulate both migration and adhesion of cancer cells through the modulation of RhoGTPases. RESULTS: We show that different concentrations of SDF-1α modulate the balance of adhesion and migration in cancer cells. Increased migration was obtained at 50 and 100 ng/ml of SDF-1α; however migration was reduced at 200 ng/ml. The adhesion between breast cancer cells and BMHC was significantly increased by SDF-1α treatment at 200 ng/ml and reduced using a blocking monoclonal antibody against CXCR4. We showed that at low SDF-1α concentration, RhoA was activated and overexpressed, while at high concentration Rac1 was promoting SDF-1α mediating-cell adhesion. CONCLUSION: We conclude that SDF-1α concentration modulates migration and adhesion of breast cancer cells, by controlling expression and activation of RhoGTPases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12885-015-1556-7) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4522077 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-45220772015-08-02 SDF-1alpha concentration dependent modulation of RhoA and Rac1 modifies breast cancer and stromal cells interaction Pasquier, Jennifer Abu-Kaoud, Nadine Abdesselem, Houari Madani, Aisha Hoarau-Véchot, Jessica Thawadi, Hamda Al. Vidal, Fabien Couderc, Bettina Favre, Gilles Rafii, Arash BMC Cancer Research Article BACKGROUND: The interaction of SDF-1alpha with its receptor CXCR4 plays a role in the occurrence of distant metastasis in many solid tumors. This interaction increases migration from primary sites as well as homing at distant sites. METHODS: Here we investigated how SDF-1α could modulate both migration and adhesion of cancer cells through the modulation of RhoGTPases. RESULTS: We show that different concentrations of SDF-1α modulate the balance of adhesion and migration in cancer cells. Increased migration was obtained at 50 and 100 ng/ml of SDF-1α; however migration was reduced at 200 ng/ml. The adhesion between breast cancer cells and BMHC was significantly increased by SDF-1α treatment at 200 ng/ml and reduced using a blocking monoclonal antibody against CXCR4. We showed that at low SDF-1α concentration, RhoA was activated and overexpressed, while at high concentration Rac1 was promoting SDF-1α mediating-cell adhesion. CONCLUSION: We conclude that SDF-1α concentration modulates migration and adhesion of breast cancer cells, by controlling expression and activation of RhoGTPases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12885-015-1556-7) contains supplementary material, which is available to authorized users. BioMed Central 2015-08-01 /pmc/articles/PMC4522077/ /pubmed/26231656 http://dx.doi.org/10.1186/s12885-015-1556-7 Text en © Pasquier et al. 2015 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Pasquier, Jennifer Abu-Kaoud, Nadine Abdesselem, Houari Madani, Aisha Hoarau-Véchot, Jessica Thawadi, Hamda Al. Vidal, Fabien Couderc, Bettina Favre, Gilles Rafii, Arash SDF-1alpha concentration dependent modulation of RhoA and Rac1 modifies breast cancer and stromal cells interaction |
title | SDF-1alpha concentration dependent modulation of RhoA and Rac1 modifies breast cancer and stromal cells interaction |
title_full | SDF-1alpha concentration dependent modulation of RhoA and Rac1 modifies breast cancer and stromal cells interaction |
title_fullStr | SDF-1alpha concentration dependent modulation of RhoA and Rac1 modifies breast cancer and stromal cells interaction |
title_full_unstemmed | SDF-1alpha concentration dependent modulation of RhoA and Rac1 modifies breast cancer and stromal cells interaction |
title_short | SDF-1alpha concentration dependent modulation of RhoA and Rac1 modifies breast cancer and stromal cells interaction |
title_sort | sdf-1alpha concentration dependent modulation of rhoa and rac1 modifies breast cancer and stromal cells interaction |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4522077/ https://www.ncbi.nlm.nih.gov/pubmed/26231656 http://dx.doi.org/10.1186/s12885-015-1556-7 |
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