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The roles and mechanism of IFIT5 in bladder cancer epithelial–mesenchymal transition and progression
The prognosis of bladder cancer (BCa) depends on several key factors including anatomical site, tumor grade, and stage. In general, muscle-invasive bladder cancer (MIBC) is associated with higher incidence of distant metastasis compared with Non-muscle-invasive bladder cancer (NMIBC). Treatment outc...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6547745/ https://www.ncbi.nlm.nih.gov/pubmed/31164632 http://dx.doi.org/10.1038/s41419-019-1669-z |
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author | Huang, Jun Lo, U-Ging Wu, Shiqi Wang, Bin Pong, Rey-Chen Lai, Chih-Ho Lin, Ho He, Dalin Hsieh, Jer-Tsong Wu, Kaijie |
author_facet | Huang, Jun Lo, U-Ging Wu, Shiqi Wang, Bin Pong, Rey-Chen Lai, Chih-Ho Lin, Ho He, Dalin Hsieh, Jer-Tsong Wu, Kaijie |
author_sort | Huang, Jun |
collection | PubMed |
description | The prognosis of bladder cancer (BCa) depends on several key factors including anatomical site, tumor grade, and stage. In general, muscle-invasive bladder cancer (MIBC) is associated with higher incidence of distant metastasis compared with Non-muscle-invasive bladder cancer (NMIBC). Treatment outcome of the patients with metastatic BCa has been very poor with ~15% of overall survival rate. Thus, it is apparently important to understand the underlying biology for metastatic progression of BCa. Although epithelial–mesenchymal transition (EMT) has long been implicated in BCa metastasis and treatment resistance, the underlying mechanism is not fully understood. In this study, we have identified that the expression of interferon induced protein with tetratricopeptide repeats 5 (IFIT5) is positively correlated with pathological characteristics, and predicts a poor prognosis of BCa patients. Since the function of IFIT5 in BCa has not yet been characterized, we demonstrate that IFIT5 can induce EMT, promote cell migration and invasion, and increase the expression of ICAM1 in BCa via down-regulation of mature miR-99a. Moreover, ICAM1 is shown as a direct target of miR-99a. Overall, we conclude that IFIT5 is a new oncogene in BCa. |
format | Online Article Text |
id | pubmed-6547745 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-65477452019-06-17 The roles and mechanism of IFIT5 in bladder cancer epithelial–mesenchymal transition and progression Huang, Jun Lo, U-Ging Wu, Shiqi Wang, Bin Pong, Rey-Chen Lai, Chih-Ho Lin, Ho He, Dalin Hsieh, Jer-Tsong Wu, Kaijie Cell Death Dis Article The prognosis of bladder cancer (BCa) depends on several key factors including anatomical site, tumor grade, and stage. In general, muscle-invasive bladder cancer (MIBC) is associated with higher incidence of distant metastasis compared with Non-muscle-invasive bladder cancer (NMIBC). Treatment outcome of the patients with metastatic BCa has been very poor with ~15% of overall survival rate. Thus, it is apparently important to understand the underlying biology for metastatic progression of BCa. Although epithelial–mesenchymal transition (EMT) has long been implicated in BCa metastasis and treatment resistance, the underlying mechanism is not fully understood. In this study, we have identified that the expression of interferon induced protein with tetratricopeptide repeats 5 (IFIT5) is positively correlated with pathological characteristics, and predicts a poor prognosis of BCa patients. Since the function of IFIT5 in BCa has not yet been characterized, we demonstrate that IFIT5 can induce EMT, promote cell migration and invasion, and increase the expression of ICAM1 in BCa via down-regulation of mature miR-99a. Moreover, ICAM1 is shown as a direct target of miR-99a. Overall, we conclude that IFIT5 is a new oncogene in BCa. Nature Publishing Group UK 2019-06-04 /pmc/articles/PMC6547745/ /pubmed/31164632 http://dx.doi.org/10.1038/s41419-019-1669-z Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Huang, Jun Lo, U-Ging Wu, Shiqi Wang, Bin Pong, Rey-Chen Lai, Chih-Ho Lin, Ho He, Dalin Hsieh, Jer-Tsong Wu, Kaijie The roles and mechanism of IFIT5 in bladder cancer epithelial–mesenchymal transition and progression |
title | The roles and mechanism of IFIT5 in bladder cancer epithelial–mesenchymal transition and progression |
title_full | The roles and mechanism of IFIT5 in bladder cancer epithelial–mesenchymal transition and progression |
title_fullStr | The roles and mechanism of IFIT5 in bladder cancer epithelial–mesenchymal transition and progression |
title_full_unstemmed | The roles and mechanism of IFIT5 in bladder cancer epithelial–mesenchymal transition and progression |
title_short | The roles and mechanism of IFIT5 in bladder cancer epithelial–mesenchymal transition and progression |
title_sort | roles and mechanism of ifit5 in bladder cancer epithelial–mesenchymal transition and progression |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6547745/ https://www.ncbi.nlm.nih.gov/pubmed/31164632 http://dx.doi.org/10.1038/s41419-019-1669-z |
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