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Specific induction of pp125 focal adhesion kinase in human breast cancer
The pp125 focal adhesion kinase (FAK) is involved in integrin-mediated cell signalling and overexpressed in a variety of solid tumours. Focal adhesion kinase expression has been correlated to invasion and metastasis, but the data on breast cancer are inconclusive. We analysed FAK mRNA, protein level...
Autores principales: | , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
2005
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361616/ https://www.ncbi.nlm.nih.gov/pubmed/16136050 http://dx.doi.org/10.1038/sj.bjc.6602744 |
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author | Watermann, D O Gabriel, B Jäger, M Orlowska-Volk, M Hasenburg, A zur Hausen, A Gitsch, G Stickeler, E |
author_facet | Watermann, D O Gabriel, B Jäger, M Orlowska-Volk, M Hasenburg, A zur Hausen, A Gitsch, G Stickeler, E |
author_sort | Watermann, D O |
collection | PubMed |
description | The pp125 focal adhesion kinase (FAK) is involved in integrin-mediated cell signalling and overexpressed in a variety of solid tumours. Focal adhesion kinase expression has been correlated to invasion and metastasis, but the data on breast cancer are inconclusive. We analysed FAK mRNA, protein levels and expression patterns in primary breast cancer and normal breast tissue. FAK expression on the functional protein level and mRNA was determined in 55 matched pairs of breast cancer and corresponding normal tissue by Western blot, immunohistochemistry and RT–PCR. Using a score ranging from 0 to +5 for Western blots, we determined in normal breast tissue a score of 1.51±0.84 (mean±standard deviation), which was strongly induced to 2.91 (±1.22) in breast cancers (P<0.001). Overall, 45 out of 55 tissue pairs (81.8%) showed this upregulation of FAK protein in tumours in comparison to normal tissue. Immunohistochemistry confirmed these findings with a significant higher score for tumours vs physiological tissue (1.0±0.63 vs 2.27±0.91; P=0.001). Interestingly, no overall significant difference in the mRNA levels (P=0.359) was observed. In conclusion, expression levels of the FAK protein are specifically upregulated in breast cancer in comparison to matched normal breast tissue supporting its pivotal role in neoplastic signal transduction and representing a potential marker for malignant transformation. |
format | Text |
id | pubmed-2361616 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2005 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-23616162009-09-10 Specific induction of pp125 focal adhesion kinase in human breast cancer Watermann, D O Gabriel, B Jäger, M Orlowska-Volk, M Hasenburg, A zur Hausen, A Gitsch, G Stickeler, E Br J Cancer Molecular Diagnostics The pp125 focal adhesion kinase (FAK) is involved in integrin-mediated cell signalling and overexpressed in a variety of solid tumours. Focal adhesion kinase expression has been correlated to invasion and metastasis, but the data on breast cancer are inconclusive. We analysed FAK mRNA, protein levels and expression patterns in primary breast cancer and normal breast tissue. FAK expression on the functional protein level and mRNA was determined in 55 matched pairs of breast cancer and corresponding normal tissue by Western blot, immunohistochemistry and RT–PCR. Using a score ranging from 0 to +5 for Western blots, we determined in normal breast tissue a score of 1.51±0.84 (mean±standard deviation), which was strongly induced to 2.91 (±1.22) in breast cancers (P<0.001). Overall, 45 out of 55 tissue pairs (81.8%) showed this upregulation of FAK protein in tumours in comparison to normal tissue. Immunohistochemistry confirmed these findings with a significant higher score for tumours vs physiological tissue (1.0±0.63 vs 2.27±0.91; P=0.001). Interestingly, no overall significant difference in the mRNA levels (P=0.359) was observed. In conclusion, expression levels of the FAK protein are specifically upregulated in breast cancer in comparison to matched normal breast tissue supporting its pivotal role in neoplastic signal transduction and representing a potential marker for malignant transformation. Nature Publishing Group 2005-09-19 2005-08-23 /pmc/articles/PMC2361616/ /pubmed/16136050 http://dx.doi.org/10.1038/sj.bjc.6602744 Text en Copyright © 2005 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 Diagnostics Watermann, D O Gabriel, B Jäger, M Orlowska-Volk, M Hasenburg, A zur Hausen, A Gitsch, G Stickeler, E Specific induction of pp125 focal adhesion kinase in human breast cancer |
title | Specific induction of pp125 focal adhesion kinase in human breast cancer |
title_full | Specific induction of pp125 focal adhesion kinase in human breast cancer |
title_fullStr | Specific induction of pp125 focal adhesion kinase in human breast cancer |
title_full_unstemmed | Specific induction of pp125 focal adhesion kinase in human breast cancer |
title_short | Specific induction of pp125 focal adhesion kinase in human breast cancer |
title_sort | specific induction of pp125 focal adhesion kinase in human breast cancer |
topic | Molecular Diagnostics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361616/ https://www.ncbi.nlm.nih.gov/pubmed/16136050 http://dx.doi.org/10.1038/sj.bjc.6602744 |
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