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MT1-MMP promotes the proliferation and invasion of gastric carcinoma cells via regulating vimentin and E-cadherin
The present study aimed to explore the possible effects of membrane-type 1 matrix metalloproteinase (MT1-MMP) on gastric carcinoma cells proliferation and invasion. Immunohistochemistry analysis was conducted to measure MT1-MMP expression level in 15 patients with gastric carcinoma. Subsequently, re...
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/PMC6423635/ https://www.ncbi.nlm.nih.gov/pubmed/30720114 http://dx.doi.org/10.3892/mmr.2019.9918 |
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author | Li, Bo Lou, Guochun Zhou, Juying |
author_facet | Li, Bo Lou, Guochun Zhou, Juying |
author_sort | Li, Bo |
collection | PubMed |
description | The present study aimed to explore the possible effects of membrane-type 1 matrix metalloproteinase (MT1-MMP) on gastric carcinoma cells proliferation and invasion. Immunohistochemistry analysis was conducted to measure MT1-MMP expression level in 15 patients with gastric carcinoma. Subsequently, recombinant short hairpin RNA (shRNA) vectors targeting MT1-MMP were constructed to silence the expression of MT1-MMP in gastric carcinoma cells. Then, the inhibitive efficiency was verified via reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. The effects of MT1-MMP silencing on cell proliferation and invasion were detected through Cell Counting Kit-8 test and Transwell assays. The expression levels of vimentin and epithelial cadherin (E-cadherin) were detected by RT-qPCR. The immunohistochemistry analysis results revealed that MT1-MMP expression in gastric carcinoma tissues was markedly overexpressed compared with non-cancerous adjacent tissues. The MT1-MMP expression level in cancer-derived cell line AGS cells was also significantly increased compared with that in non-cancer-derived GES-1 cells. In addition, the MT1-MMP expression level in AGS cells was significantly decreased via shRNA transfection. Cell proliferation and invasion were markedly inhibited following knockdown of MT1-MMP level in AGS cells. These inhibitory effects were associated with the decreased expression of vimentin and increased expression of E-cadherin. MT1-MMP was overexpressed in gastric carcinoma cells, and silencing of MT1-MMP inhibited the proliferation and invasion of cells via regulating the expression of vimentin and E-cadherin. |
format | Online Article Text |
id | pubmed-6423635 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-64236352019-03-22 MT1-MMP promotes the proliferation and invasion of gastric carcinoma cells via regulating vimentin and E-cadherin Li, Bo Lou, Guochun Zhou, Juying Mol Med Rep Articles The present study aimed to explore the possible effects of membrane-type 1 matrix metalloproteinase (MT1-MMP) on gastric carcinoma cells proliferation and invasion. Immunohistochemistry analysis was conducted to measure MT1-MMP expression level in 15 patients with gastric carcinoma. Subsequently, recombinant short hairpin RNA (shRNA) vectors targeting MT1-MMP were constructed to silence the expression of MT1-MMP in gastric carcinoma cells. Then, the inhibitive efficiency was verified via reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. The effects of MT1-MMP silencing on cell proliferation and invasion were detected through Cell Counting Kit-8 test and Transwell assays. The expression levels of vimentin and epithelial cadherin (E-cadherin) were detected by RT-qPCR. The immunohistochemistry analysis results revealed that MT1-MMP expression in gastric carcinoma tissues was markedly overexpressed compared with non-cancerous adjacent tissues. The MT1-MMP expression level in cancer-derived cell line AGS cells was also significantly increased compared with that in non-cancer-derived GES-1 cells. In addition, the MT1-MMP expression level in AGS cells was significantly decreased via shRNA transfection. Cell proliferation and invasion were markedly inhibited following knockdown of MT1-MMP level in AGS cells. These inhibitory effects were associated with the decreased expression of vimentin and increased expression of E-cadherin. MT1-MMP was overexpressed in gastric carcinoma cells, and silencing of MT1-MMP inhibited the proliferation and invasion of cells via regulating the expression of vimentin and E-cadherin. D.A. Spandidos 2019-04 2019-01-31 /pmc/articles/PMC6423635/ /pubmed/30720114 http://dx.doi.org/10.3892/mmr.2019.9918 Text en Copyright: © Li 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 Li, Bo Lou, Guochun Zhou, Juying MT1-MMP promotes the proliferation and invasion of gastric carcinoma cells via regulating vimentin and E-cadherin |
title | MT1-MMP promotes the proliferation and invasion of gastric carcinoma cells via regulating vimentin and E-cadherin |
title_full | MT1-MMP promotes the proliferation and invasion of gastric carcinoma cells via regulating vimentin and E-cadherin |
title_fullStr | MT1-MMP promotes the proliferation and invasion of gastric carcinoma cells via regulating vimentin and E-cadherin |
title_full_unstemmed | MT1-MMP promotes the proliferation and invasion of gastric carcinoma cells via regulating vimentin and E-cadherin |
title_short | MT1-MMP promotes the proliferation and invasion of gastric carcinoma cells via regulating vimentin and E-cadherin |
title_sort | mt1-mmp promotes the proliferation and invasion of gastric carcinoma cells via regulating vimentin and e-cadherin |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6423635/ https://www.ncbi.nlm.nih.gov/pubmed/30720114 http://dx.doi.org/10.3892/mmr.2019.9918 |
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