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GDF15 promotes EMT and metastasis in colorectal cancer
Metastasis is the major cause of cancer deaths, and the epithelial–mesenchymal transition (EMT) has been considered to be a fundamental event in cancer metastasis. However, the role of growth differentiation factor 15 (GDF15) in colorectal cancer (CRC) metastasis and EMT remains poorly understood. H...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4808038/ https://www.ncbi.nlm.nih.gov/pubmed/26497212 |
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author | Li, Chen Wang, Jingyu Kong, Jianlu Tang, Jinlong Wu, Yihua Xu, Enping Zhang, Honghe Lai, Maode |
author_facet | Li, Chen Wang, Jingyu Kong, Jianlu Tang, Jinlong Wu, Yihua Xu, Enping Zhang, Honghe Lai, Maode |
author_sort | Li, Chen |
collection | PubMed |
description | Metastasis is the major cause of cancer deaths, and the epithelial–mesenchymal transition (EMT) has been considered to be a fundamental event in cancer metastasis. However, the role of growth differentiation factor 15 (GDF15) in colorectal cancer (CRC) metastasis and EMT remains poorly understood. Here, we showed that GDF15 promoted CRC cell metastasis both in vitro and in vivo. In addition, the EMT process was enhanced by GDF15 through binding to TGF-β receptor to activate Smad2 and Smad3 pathways. Clinical data showed GDF15 level in tumor tissues, and the serum was significantly increased, in which high GDF15 level correlated with a reduced overall survival in CRC. Thus, GDF15 may promote colorectal cancer metastasis through activating EMT. Promisingly, GDF15 could be considered as a novel prognostic marker for CRC in the clinic. |
format | Online Article Text |
id | pubmed-4808038 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-48080382016-04-19 GDF15 promotes EMT and metastasis in colorectal cancer Li, Chen Wang, Jingyu Kong, Jianlu Tang, Jinlong Wu, Yihua Xu, Enping Zhang, Honghe Lai, Maode Oncotarget Research Paper Metastasis is the major cause of cancer deaths, and the epithelial–mesenchymal transition (EMT) has been considered to be a fundamental event in cancer metastasis. However, the role of growth differentiation factor 15 (GDF15) in colorectal cancer (CRC) metastasis and EMT remains poorly understood. Here, we showed that GDF15 promoted CRC cell metastasis both in vitro and in vivo. In addition, the EMT process was enhanced by GDF15 through binding to TGF-β receptor to activate Smad2 and Smad3 pathways. Clinical data showed GDF15 level in tumor tissues, and the serum was significantly increased, in which high GDF15 level correlated with a reduced overall survival in CRC. Thus, GDF15 may promote colorectal cancer metastasis through activating EMT. Promisingly, GDF15 could be considered as a novel prognostic marker for CRC in the clinic. Impact Journals LLC 2015-10-22 /pmc/articles/PMC4808038/ /pubmed/26497212 Text en Copyright: © 2016 Li et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Li, Chen Wang, Jingyu Kong, Jianlu Tang, Jinlong Wu, Yihua Xu, Enping Zhang, Honghe Lai, Maode GDF15 promotes EMT and metastasis in colorectal cancer |
title | GDF15 promotes EMT and metastasis in colorectal cancer |
title_full | GDF15 promotes EMT and metastasis in colorectal cancer |
title_fullStr | GDF15 promotes EMT and metastasis in colorectal cancer |
title_full_unstemmed | GDF15 promotes EMT and metastasis in colorectal cancer |
title_short | GDF15 promotes EMT and metastasis in colorectal cancer |
title_sort | gdf15 promotes emt and metastasis in colorectal cancer |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4808038/ https://www.ncbi.nlm.nih.gov/pubmed/26497212 |
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