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Identification of differentially expressed proteins in the gastric mucosal atypical hyperplasia tissue microenvironment
In the present study, the interaction of proteins in the microenvironment of gastric mucosal atypical hyperplasia was analyzed. The stromata of normal gastric mucosa (NGM) and gastric mucosal atypical hyperplasia (GMAH) tissues were purified with laser capture microdissection (LCM). The differential...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6036401/ https://www.ncbi.nlm.nih.gov/pubmed/30008939 http://dx.doi.org/10.3892/ol.2018.8941 |
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author | Zhang, He-Liang Liu, Chong-Yuan Ma, Wei Huang, Lin Li, Chang-Jian Li, Cheng-Song Zhang, Zhi-Wei |
author_facet | Zhang, He-Liang Liu, Chong-Yuan Ma, Wei Huang, Lin Li, Chang-Jian Li, Cheng-Song Zhang, Zhi-Wei |
author_sort | Zhang, He-Liang |
collection | PubMed |
description | In the present study, the interaction of proteins in the microenvironment of gastric mucosal atypical hyperplasia was analyzed. The stromata of normal gastric mucosa (NGM) and gastric mucosal atypical hyperplasia (GMAH) tissues were purified with laser capture microdissection (LCM). The differentially expressed GMAH proteins of the NGM and GMAH tissues were identified by quantitative proteomic techniques with isotope labeling. The cross-talk between differentially expressed proteins in NGM and GMAH tissues was then analyzed by bioinformatics. There were 165 differentially expressed proteins identified from the stromata of NGM and GMAH tissues. Among them, 99 proteins were upregulated and 66 were downregulated in GMAH tissue. The present study demonstrated that these proteins in gastric mucosal atypical hyperplasia were involved in cancer-associated signaling pathways, including the p53, mitogen-activated protein kinase (MAPK), cell cycle and apoptosis signaling pathways, and were involved in cellular growth, cellular proliferation, apoptosis and the humoral immune response. The results of the present study suggest that the 165 differentially expressed proteins, including S100 calcium-binding protein A6 (S100A6) and superoxide dismutase 3 (SOD3) in the microenvironment of gastric mucosal atypical hyperplasia, are involved in the p53, MAPK, cell cycle and apoptosis signaling pathways, and serve a function in the pathogenesis of gastric cancer. |
format | Online Article Text |
id | pubmed-6036401 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-60364012018-07-15 Identification of differentially expressed proteins in the gastric mucosal atypical hyperplasia tissue microenvironment Zhang, He-Liang Liu, Chong-Yuan Ma, Wei Huang, Lin Li, Chang-Jian Li, Cheng-Song Zhang, Zhi-Wei Oncol Lett Articles In the present study, the interaction of proteins in the microenvironment of gastric mucosal atypical hyperplasia was analyzed. The stromata of normal gastric mucosa (NGM) and gastric mucosal atypical hyperplasia (GMAH) tissues were purified with laser capture microdissection (LCM). The differentially expressed GMAH proteins of the NGM and GMAH tissues were identified by quantitative proteomic techniques with isotope labeling. The cross-talk between differentially expressed proteins in NGM and GMAH tissues was then analyzed by bioinformatics. There were 165 differentially expressed proteins identified from the stromata of NGM and GMAH tissues. Among them, 99 proteins were upregulated and 66 were downregulated in GMAH tissue. The present study demonstrated that these proteins in gastric mucosal atypical hyperplasia were involved in cancer-associated signaling pathways, including the p53, mitogen-activated protein kinase (MAPK), cell cycle and apoptosis signaling pathways, and were involved in cellular growth, cellular proliferation, apoptosis and the humoral immune response. The results of the present study suggest that the 165 differentially expressed proteins, including S100 calcium-binding protein A6 (S100A6) and superoxide dismutase 3 (SOD3) in the microenvironment of gastric mucosal atypical hyperplasia, are involved in the p53, MAPK, cell cycle and apoptosis signaling pathways, and serve a function in the pathogenesis of gastric cancer. D.A. Spandidos 2018-08 2018-06-11 /pmc/articles/PMC6036401/ /pubmed/30008939 http://dx.doi.org/10.3892/ol.2018.8941 Text en Copyright: © Zhang 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 Zhang, He-Liang Liu, Chong-Yuan Ma, Wei Huang, Lin Li, Chang-Jian Li, Cheng-Song Zhang, Zhi-Wei Identification of differentially expressed proteins in the gastric mucosal atypical hyperplasia tissue microenvironment |
title | Identification of differentially expressed proteins in the gastric mucosal atypical hyperplasia tissue microenvironment |
title_full | Identification of differentially expressed proteins in the gastric mucosal atypical hyperplasia tissue microenvironment |
title_fullStr | Identification of differentially expressed proteins in the gastric mucosal atypical hyperplasia tissue microenvironment |
title_full_unstemmed | Identification of differentially expressed proteins in the gastric mucosal atypical hyperplasia tissue microenvironment |
title_short | Identification of differentially expressed proteins in the gastric mucosal atypical hyperplasia tissue microenvironment |
title_sort | identification of differentially expressed proteins in the gastric mucosal atypical hyperplasia tissue microenvironment |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6036401/ https://www.ncbi.nlm.nih.gov/pubmed/30008939 http://dx.doi.org/10.3892/ol.2018.8941 |
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