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Enhanced progression of human prostate cancer PC3 cells induced by the microenvironment of the seminal vesicle
The objective of this study was to characterise the mechanism mediating the prostate cancer progression induced by the microenvironment of seminal vesicle (SV). The invasive potential of PC3 cells significantly increased after treatment with extract from SV of NOD/SCID mouse. Among several growth fa...
Autores principales: | , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
2008
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361452/ https://www.ncbi.nlm.nih.gov/pubmed/18182987 http://dx.doi.org/10.1038/sj.bjc.6604169 |
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author | Kumano, M Miyake, H Kurahashi, T Yamanaka, K Fujisawa, M |
author_facet | Kumano, M Miyake, H Kurahashi, T Yamanaka, K Fujisawa, M |
author_sort | Kumano, M |
collection | PubMed |
description | The objective of this study was to characterise the mechanism mediating the prostate cancer progression induced by the microenvironment of seminal vesicle (SV). The invasive potential of PC3 cells significantly increased after treatment with extract from SV of NOD/SCID mouse. Among several growth factors and cytokines that were present in the SV extract, transforming growth factor-β(1) (TGF-β(1)) significantly enhanced the invasive potential of PC3 cells; however, the additional treatment with neutralising antibody against TGF-β(1) suppressed the enhanced invasive potential induced by the SV extract. Changes in the invasive potential in PC3 cells after treatment with the SV extract and/or TGF-β(1) were in proportion to those in the production of urokinase-type plasminogen activator (uPA) by PC3 cells. Tumour growth as well as the incidence of lymph node metastasis in NOD/SCID mice after the injection of PC3 cells into the SV were significantly greater than those after the injection into the prostate. These findings suggest that the microenvironment of SV enhances the progression of prostate cancer through a stimulated invasive potential, and that enhanced uPA production in prostate cancer cells induced by TGF-β(1) could therefore be one of the most important mechanisms involved in the progression of prostate cancer after SV invasion. |
format | Text |
id | pubmed-2361452 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-23614522009-09-10 Enhanced progression of human prostate cancer PC3 cells induced by the microenvironment of the seminal vesicle Kumano, M Miyake, H Kurahashi, T Yamanaka, K Fujisawa, M Br J Cancer Translational Therapeutics The objective of this study was to characterise the mechanism mediating the prostate cancer progression induced by the microenvironment of seminal vesicle (SV). The invasive potential of PC3 cells significantly increased after treatment with extract from SV of NOD/SCID mouse. Among several growth factors and cytokines that were present in the SV extract, transforming growth factor-β(1) (TGF-β(1)) significantly enhanced the invasive potential of PC3 cells; however, the additional treatment with neutralising antibody against TGF-β(1) suppressed the enhanced invasive potential induced by the SV extract. Changes in the invasive potential in PC3 cells after treatment with the SV extract and/or TGF-β(1) were in proportion to those in the production of urokinase-type plasminogen activator (uPA) by PC3 cells. Tumour growth as well as the incidence of lymph node metastasis in NOD/SCID mice after the injection of PC3 cells into the SV were significantly greater than those after the injection into the prostate. These findings suggest that the microenvironment of SV enhances the progression of prostate cancer through a stimulated invasive potential, and that enhanced uPA production in prostate cancer cells induced by TGF-β(1) could therefore be one of the most important mechanisms involved in the progression of prostate cancer after SV invasion. Nature Publishing Group 2008-01-29 2008-01-08 /pmc/articles/PMC2361452/ /pubmed/18182987 http://dx.doi.org/10.1038/sj.bjc.6604169 Text en Copyright © 2008 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 | Translational Therapeutics Kumano, M Miyake, H Kurahashi, T Yamanaka, K Fujisawa, M Enhanced progression of human prostate cancer PC3 cells induced by the microenvironment of the seminal vesicle |
title | Enhanced progression of human prostate cancer PC3 cells induced by the microenvironment of the seminal vesicle |
title_full | Enhanced progression of human prostate cancer PC3 cells induced by the microenvironment of the seminal vesicle |
title_fullStr | Enhanced progression of human prostate cancer PC3 cells induced by the microenvironment of the seminal vesicle |
title_full_unstemmed | Enhanced progression of human prostate cancer PC3 cells induced by the microenvironment of the seminal vesicle |
title_short | Enhanced progression of human prostate cancer PC3 cells induced by the microenvironment of the seminal vesicle |
title_sort | enhanced progression of human prostate cancer pc3 cells induced by the microenvironment of the seminal vesicle |
topic | Translational Therapeutics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361452/ https://www.ncbi.nlm.nih.gov/pubmed/18182987 http://dx.doi.org/10.1038/sj.bjc.6604169 |
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