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Periostin promotes epithelial-mesenchymal transition via the MAPK/miR-381 axis in lung cancer
Periostin (POSTN, PN, or osteoblast-specific factor OSF-2) is a multifunctional cytokine that signals between the cell and the extracellular matrix. Periostin plays an important role in tumor development and is involved in carcinoma cell epithelial-mesenchymal transition (EMT), whereby mature epithe...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5617502/ https://www.ncbi.nlm.nih.gov/pubmed/28977942 http://dx.doi.org/10.18632/oncotarget.19273 |
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author | Hu, Wei-Wei Chen, Po-Chun Chen, Jun-Ming Wu, Yue-Ming Liu, Po-Yi Lu, Chih-Hao Lin, Yu-Feng Tang, Chih-Hsin Chao, Chia-Chia |
author_facet | Hu, Wei-Wei Chen, Po-Chun Chen, Jun-Ming Wu, Yue-Ming Liu, Po-Yi Lu, Chih-Hao Lin, Yu-Feng Tang, Chih-Hsin Chao, Chia-Chia |
author_sort | Hu, Wei-Wei |
collection | PubMed |
description | Periostin (POSTN, PN, or osteoblast-specific factor OSF-2) is a multifunctional cytokine that signals between the cell and the extracellular matrix. Periostin plays an important role in tumor development and is involved in carcinoma cell epithelial-mesenchymal transition (EMT), whereby mature epithelial cells undergo phenotypic morphological changes and become invasive, motile cells. Here, we discuss the molecular mechanisms involved in periostin-induced promotion of EMT in lung cancer cells. Online TCGA datasets demonstrate the prognostic relevance of periostin in lung cancer; a higher periostin level correlates with poor overall survival. Similarly, our IHC results show that high periostin expression is positively correlated with the EMT markers Snail and Twist, as well as stage of lung cancer. We found that recombinant periostin induces the EMT phenotype in lung cancer cells through the p38/ERK pathway, while pretreatment with chemical inhibitors prevented periostin-induced EMT induction. Moreover, we found that periostin regulates EMT by repressing microRNA-381 (miR-381) expression, which targets both Snail and Twist. Using the miR-381 mimic, we dramatically reversed periostin-induced Snail and Twist expression. Furthermore, periostin knockdown dramatically affected EMT markers and cell migration potential. The role of periostin in lung cancer progression is elucidated by the in vivo mouse model. Our findings indicate that changes in periostin expression in lung cancer may serve as a therapeutic target for the treatment of lung cancer metastasis. |
format | Online Article Text |
id | pubmed-5617502 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-56175022017-10-03 Periostin promotes epithelial-mesenchymal transition via the MAPK/miR-381 axis in lung cancer Hu, Wei-Wei Chen, Po-Chun Chen, Jun-Ming Wu, Yue-Ming Liu, Po-Yi Lu, Chih-Hao Lin, Yu-Feng Tang, Chih-Hsin Chao, Chia-Chia Oncotarget Research Paper Periostin (POSTN, PN, or osteoblast-specific factor OSF-2) is a multifunctional cytokine that signals between the cell and the extracellular matrix. Periostin plays an important role in tumor development and is involved in carcinoma cell epithelial-mesenchymal transition (EMT), whereby mature epithelial cells undergo phenotypic morphological changes and become invasive, motile cells. Here, we discuss the molecular mechanisms involved in periostin-induced promotion of EMT in lung cancer cells. Online TCGA datasets demonstrate the prognostic relevance of periostin in lung cancer; a higher periostin level correlates with poor overall survival. Similarly, our IHC results show that high periostin expression is positively correlated with the EMT markers Snail and Twist, as well as stage of lung cancer. We found that recombinant periostin induces the EMT phenotype in lung cancer cells through the p38/ERK pathway, while pretreatment with chemical inhibitors prevented periostin-induced EMT induction. Moreover, we found that periostin regulates EMT by repressing microRNA-381 (miR-381) expression, which targets both Snail and Twist. Using the miR-381 mimic, we dramatically reversed periostin-induced Snail and Twist expression. Furthermore, periostin knockdown dramatically affected EMT markers and cell migration potential. The role of periostin in lung cancer progression is elucidated by the in vivo mouse model. Our findings indicate that changes in periostin expression in lung cancer may serve as a therapeutic target for the treatment of lung cancer metastasis. Impact Journals LLC 2017-07-15 /pmc/articles/PMC5617502/ /pubmed/28977942 http://dx.doi.org/10.18632/oncotarget.19273 Text en Copyright: © 2017 Hu et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Hu, Wei-Wei Chen, Po-Chun Chen, Jun-Ming Wu, Yue-Ming Liu, Po-Yi Lu, Chih-Hao Lin, Yu-Feng Tang, Chih-Hsin Chao, Chia-Chia Periostin promotes epithelial-mesenchymal transition via the MAPK/miR-381 axis in lung cancer |
title | Periostin promotes epithelial-mesenchymal transition via the MAPK/miR-381 axis in lung cancer |
title_full | Periostin promotes epithelial-mesenchymal transition via the MAPK/miR-381 axis in lung cancer |
title_fullStr | Periostin promotes epithelial-mesenchymal transition via the MAPK/miR-381 axis in lung cancer |
title_full_unstemmed | Periostin promotes epithelial-mesenchymal transition via the MAPK/miR-381 axis in lung cancer |
title_short | Periostin promotes epithelial-mesenchymal transition via the MAPK/miR-381 axis in lung cancer |
title_sort | periostin promotes epithelial-mesenchymal transition via the mapk/mir-381 axis in lung cancer |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5617502/ https://www.ncbi.nlm.nih.gov/pubmed/28977942 http://dx.doi.org/10.18632/oncotarget.19273 |
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