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miR-25 promotes invasion of human non-small cell lung cancer via CDH1

MicroRNA-25 (miR-25) has been reported to be overexpressed in numerous human tumors and plays a key role in tumor promotor. However, there are few reports about miR-25 expression and function in non-small cell lung cancer (NSCLC). In this study, we investigated the biological role of miR-25 in NSCLC...

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Detalles Bibliográficos
Autores principales: Liu, Bing, Sun, Xuerong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6629186/
https://www.ncbi.nlm.nih.gov/pubmed/31208279
http://dx.doi.org/10.1080/21655979.2019.1632668
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author Liu, Bing
Sun, Xuerong
author_facet Liu, Bing
Sun, Xuerong
author_sort Liu, Bing
collection PubMed
description MicroRNA-25 (miR-25) has been reported to be overexpressed in numerous human tumors and plays a key role in tumor promotor. However, there are few reports about miR-25 expression and function in non-small cell lung cancer (NSCLC). In this study, we investigated the biological role of miR-25 in NSCLC and its underlying molecular mechanisms. We found that the upregulation of miR-25 was correlated with lymph node metastasis and TNM stage in 113 NSCLC patients. Moreover, the up-regulation of miR-25 was associated with poor survival of NSCLC patients and might be used as an independent prognostic factor. Moreover, forced expression of miR-25 enhanced H358 and Calu-1 cell migration and invasion, but not apoptosis and proliferation in vitro. Elevation of invasion and metastasis by miR-25 directly and significantly correlated with inactivation of CDH1 expression. Therefore, patients with up-regulated miR-25 are prone to lymph node metastasis and thus have a poor prognosis.
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spelling pubmed-66291862020-07-06 miR-25 promotes invasion of human non-small cell lung cancer via CDH1 Liu, Bing Sun, Xuerong Bioengineered Research Paper MicroRNA-25 (miR-25) has been reported to be overexpressed in numerous human tumors and plays a key role in tumor promotor. However, there are few reports about miR-25 expression and function in non-small cell lung cancer (NSCLC). In this study, we investigated the biological role of miR-25 in NSCLC and its underlying molecular mechanisms. We found that the upregulation of miR-25 was correlated with lymph node metastasis and TNM stage in 113 NSCLC patients. Moreover, the up-regulation of miR-25 was associated with poor survival of NSCLC patients and might be used as an independent prognostic factor. Moreover, forced expression of miR-25 enhanced H358 and Calu-1 cell migration and invasion, but not apoptosis and proliferation in vitro. Elevation of invasion and metastasis by miR-25 directly and significantly correlated with inactivation of CDH1 expression. Therefore, patients with up-regulated miR-25 are prone to lymph node metastasis and thus have a poor prognosis. Taylor & Francis 2019-07-06 /pmc/articles/PMC6629186/ /pubmed/31208279 http://dx.doi.org/10.1080/21655979.2019.1632668 Text en © 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Liu, Bing
Sun, Xuerong
miR-25 promotes invasion of human non-small cell lung cancer via CDH1
title miR-25 promotes invasion of human non-small cell lung cancer via CDH1
title_full miR-25 promotes invasion of human non-small cell lung cancer via CDH1
title_fullStr miR-25 promotes invasion of human non-small cell lung cancer via CDH1
title_full_unstemmed miR-25 promotes invasion of human non-small cell lung cancer via CDH1
title_short miR-25 promotes invasion of human non-small cell lung cancer via CDH1
title_sort mir-25 promotes invasion of human non-small cell lung cancer via cdh1
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6629186/
https://www.ncbi.nlm.nih.gov/pubmed/31208279
http://dx.doi.org/10.1080/21655979.2019.1632668
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