PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway
Liver metastasis is one of the major causes of death in patients with colorectal cancer, and although treatment has improved recently, the long-term survival rate of patients has not improved significantly. In the present study, we used immunohistochemistry to determine that phosphoprotein enriched...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6278416/ https://www.ncbi.nlm.nih.gov/pubmed/30365128 http://dx.doi.org/10.3892/or.2018.6825 |
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author | Tang, Bo Liang, Wenjin Liao, Yong Li, Zeming Wang, Yan Yan, Chao |
author_facet | Tang, Bo Liang, Wenjin Liao, Yong Li, Zeming Wang, Yan Yan, Chao |
author_sort | Tang, Bo |
collection | PubMed |
description | Liver metastasis is one of the major causes of death in patients with colorectal cancer, and although treatment has improved recently, the long-term survival rate of patients has not improved significantly. In the present study, we used immunohistochemistry to determine that phosphoprotein enriched in astrocytes-15 kDa (PEA15) was highly expressed in colorectal cancer tissues and liver metastatic cancer tissues. It was also highly expressed in metastatic colorectal cancer patients compared to non-metastatic patients. Through clinicopathological data of patients with liver metastasis of colorectal cancer, we found that high expression of PEA15 was positively correlated with TNM staging, liver metastasis and poor prognosis of colorectal cancer patients. Using confocal immunofluorescence microscopy, western blotting and cell proliferation, migration and invasion assays, we also determined that PEA15 could promote cancer cell proliferation in vitro and in vivo, epithelial mesenchymal transition (EMT) and the characteristics of cancer stem cells in vitro, thus promoting the abilities of invasion and migration. In addition, we revealed that PEA15 promoted the liver metastasis of colorectal cancer cells in a xenograft tumor metastasis model. In addition, concerning the mechanism, we used gene chip analysis to determine that PEA15 upregulated the ERK/MAPK signaling pathway in colorectal cancer cells. Therefore, we concluded that PEA15 may be a potential biomarker for liver metastasis of colorectal cancer therapy. Collectively, PEA15 promoted the development of liver metastasis of colorectal cancer through the ERK/MAPK signaling pathway. |
format | Online Article Text |
id | pubmed-6278416 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-62784162018-12-17 PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway Tang, Bo Liang, Wenjin Liao, Yong Li, Zeming Wang, Yan Yan, Chao Oncol Rep Articles Liver metastasis is one of the major causes of death in patients with colorectal cancer, and although treatment has improved recently, the long-term survival rate of patients has not improved significantly. In the present study, we used immunohistochemistry to determine that phosphoprotein enriched in astrocytes-15 kDa (PEA15) was highly expressed in colorectal cancer tissues and liver metastatic cancer tissues. It was also highly expressed in metastatic colorectal cancer patients compared to non-metastatic patients. Through clinicopathological data of patients with liver metastasis of colorectal cancer, we found that high expression of PEA15 was positively correlated with TNM staging, liver metastasis and poor prognosis of colorectal cancer patients. Using confocal immunofluorescence microscopy, western blotting and cell proliferation, migration and invasion assays, we also determined that PEA15 could promote cancer cell proliferation in vitro and in vivo, epithelial mesenchymal transition (EMT) and the characteristics of cancer stem cells in vitro, thus promoting the abilities of invasion and migration. In addition, we revealed that PEA15 promoted the liver metastasis of colorectal cancer cells in a xenograft tumor metastasis model. In addition, concerning the mechanism, we used gene chip analysis to determine that PEA15 upregulated the ERK/MAPK signaling pathway in colorectal cancer cells. Therefore, we concluded that PEA15 may be a potential biomarker for liver metastasis of colorectal cancer therapy. Collectively, PEA15 promoted the development of liver metastasis of colorectal cancer through the ERK/MAPK signaling pathway. D.A. Spandidos 2019-01 2018-10-25 /pmc/articles/PMC6278416/ /pubmed/30365128 http://dx.doi.org/10.3892/or.2018.6825 Text en Copyright: © Tang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Tang, Bo Liang, Wenjin Liao, Yong Li, Zeming Wang, Yan Yan, Chao PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway |
title | PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway |
title_full | PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway |
title_fullStr | PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway |
title_full_unstemmed | PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway |
title_short | PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway |
title_sort | pea15 promotes liver metastasis of colorectal cancer by upregulating the erk/mapk signaling pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6278416/ https://www.ncbi.nlm.nih.gov/pubmed/30365128 http://dx.doi.org/10.3892/or.2018.6825 |
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