Matrix metalloproteinase‐14 (MMP‐14) downregulation inhibits esophageal squamous cell carcinoma cell migration, invasion, and proliferation

BACKGROUND: Matrix metalloproteinase‐14 (MMP‐14) is known to be a key regulator of oncogenesis and tumor progression. The present study was designed to assess the relationship between the downregulation of MMP‐14 and the in vitro proliferative, migratory, and invasive activity of esophageal squamous...

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Autores principales: Chen, Nanzheng, Zhang, Guangjian, Fu, Junke, Wu, Qifei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons Australia, Ltd 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7606025/
https://www.ncbi.nlm.nih.gov/pubmed/32930509
http://dx.doi.org/10.1111/1759-7714.13636
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author Chen, Nanzheng
Zhang, Guangjian
Fu, Junke
Wu, Qifei
author_facet Chen, Nanzheng
Zhang, Guangjian
Fu, Junke
Wu, Qifei
author_sort Chen, Nanzheng
collection PubMed
description BACKGROUND: Matrix metalloproteinase‐14 (MMP‐14) is known to be a key regulator of oncogenesis and tumor progression. The present study was designed to assess the relationship between the downregulation of MMP‐14 and the in vitro proliferative, migratory, and invasive activity of esophageal squamous cell carcinoma (ESCC) cells. METHODS: MMP‐14 expression in human ESCC and paracancerous normal esophageal tissue samples was evaluated via immunohistochemistry, and correlations between MMP‐14 staining and patient clinicopathological features were examined. In addition, siRNA was used to knockdown MMP‐14 in ESCC cells, and the proliferation and invasive activity of these cells were then evaluated via MTT and Transwell assays, respectively. Flow cytometry was additionally used to assess cell cycle progression, while Western blotting was employed to measure protein levels within these cells. RESULTS: ESCC samples were found to exhibit MMP‐14 overexpression relative to paracancerous tissue samples, and this overexpression was positively correlated with tumor T classification (T1‐2 vs. T3; P < 0.05), N classification (negative vs. positive; P < 0.001), degree of differentiation (G1 vs. G3, P < 0.05; G2 vs. G3, P < 0.05) and clinical stage (I–IIA vs. IIB–III; P < 0.05). When MMP‐14 was knocked down in ESCC cells, this induced cell cycle arrest, impairing their proliferative and invasive activity. CONCLUSIONS: MMP‐14 is a key regulator of the proliferation and invasion of ESCC cells, making it a viable therapeutic target for the treatment of this cancer.
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spelling pubmed-76060252020-11-05 Matrix metalloproteinase‐14 (MMP‐14) downregulation inhibits esophageal squamous cell carcinoma cell migration, invasion, and proliferation Chen, Nanzheng Zhang, Guangjian Fu, Junke Wu, Qifei Thorac Cancer Original Articles BACKGROUND: Matrix metalloproteinase‐14 (MMP‐14) is known to be a key regulator of oncogenesis and tumor progression. The present study was designed to assess the relationship between the downregulation of MMP‐14 and the in vitro proliferative, migratory, and invasive activity of esophageal squamous cell carcinoma (ESCC) cells. METHODS: MMP‐14 expression in human ESCC and paracancerous normal esophageal tissue samples was evaluated via immunohistochemistry, and correlations between MMP‐14 staining and patient clinicopathological features were examined. In addition, siRNA was used to knockdown MMP‐14 in ESCC cells, and the proliferation and invasive activity of these cells were then evaluated via MTT and Transwell assays, respectively. Flow cytometry was additionally used to assess cell cycle progression, while Western blotting was employed to measure protein levels within these cells. RESULTS: ESCC samples were found to exhibit MMP‐14 overexpression relative to paracancerous tissue samples, and this overexpression was positively correlated with tumor T classification (T1‐2 vs. T3; P < 0.05), N classification (negative vs. positive; P < 0.001), degree of differentiation (G1 vs. G3, P < 0.05; G2 vs. G3, P < 0.05) and clinical stage (I–IIA vs. IIB–III; P < 0.05). When MMP‐14 was knocked down in ESCC cells, this induced cell cycle arrest, impairing their proliferative and invasive activity. CONCLUSIONS: MMP‐14 is a key regulator of the proliferation and invasion of ESCC cells, making it a viable therapeutic target for the treatment of this cancer. John Wiley & Sons Australia, Ltd 2020-09-15 2020-11 /pmc/articles/PMC7606025/ /pubmed/32930509 http://dx.doi.org/10.1111/1759-7714.13636 Text en © 2020 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Original Articles
Chen, Nanzheng
Zhang, Guangjian
Fu, Junke
Wu, Qifei
Matrix metalloproteinase‐14 (MMP‐14) downregulation inhibits esophageal squamous cell carcinoma cell migration, invasion, and proliferation
title Matrix metalloproteinase‐14 (MMP‐14) downregulation inhibits esophageal squamous cell carcinoma cell migration, invasion, and proliferation
title_full Matrix metalloproteinase‐14 (MMP‐14) downregulation inhibits esophageal squamous cell carcinoma cell migration, invasion, and proliferation
title_fullStr Matrix metalloproteinase‐14 (MMP‐14) downregulation inhibits esophageal squamous cell carcinoma cell migration, invasion, and proliferation
title_full_unstemmed Matrix metalloproteinase‐14 (MMP‐14) downregulation inhibits esophageal squamous cell carcinoma cell migration, invasion, and proliferation
title_short Matrix metalloproteinase‐14 (MMP‐14) downregulation inhibits esophageal squamous cell carcinoma cell migration, invasion, and proliferation
title_sort matrix metalloproteinase‐14 (mmp‐14) downregulation inhibits esophageal squamous cell carcinoma cell migration, invasion, and proliferation
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7606025/
https://www.ncbi.nlm.nih.gov/pubmed/32930509
http://dx.doi.org/10.1111/1759-7714.13636
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