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MiR-451 inhibits cell growth and invasion by targeting MIF and is associated with survival in nasopharyngeal carcinoma
BACKGROUND: MiRNAs play important roles in diverse biological processes including tumorigenesis. However, little is known about the function and mechanism of miR-451 in nasopharyngeal carcinoma (NPC). METHODS: Quantitative RT-PCR was used to quantify miR-451 expression in NPC cell lines and clinical...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3853142/ https://www.ncbi.nlm.nih.gov/pubmed/24138931 http://dx.doi.org/10.1186/1476-4598-12-123 |
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author | Liu, Na Jiang, Ning Guo, Rui Jiang, Wei He, Qing-Mei Xu, Ya-Fei Li, Ying-Qin Tang, Ling-Long Mao, Yan-Ping Sun, Ying Ma, Jun |
author_facet | Liu, Na Jiang, Ning Guo, Rui Jiang, Wei He, Qing-Mei Xu, Ya-Fei Li, Ying-Qin Tang, Ling-Long Mao, Yan-Ping Sun, Ying Ma, Jun |
author_sort | Liu, Na |
collection | PubMed |
description | BACKGROUND: MiRNAs play important roles in diverse biological processes including tumorigenesis. However, little is known about the function and mechanism of miR-451 in nasopharyngeal carcinoma (NPC). METHODS: Quantitative RT-PCR was used to quantify miR-451 expression in NPC cell lines and clinical tissues. Kaplan-Meier curves were used to estimate the association between miR-451 expression and survival. The MTT, colony formation, Transwell migration and invasion assays, and a xenograft model were performed. A miR-451 target was confirmed using luciferase reporter assays, quantitative RT-PCR, and Western blotting. RESULTS: MiR-451 was significantly downregulated in NPC cell lines and clinical tissues (P < 0.01). Patients with low expression of miR-451 had poorer overall survival (HR, 1.98; 95% CI, 1.16-3.34; P = 0.01) and disease-free survival (HR, 1.68; 95% CI, 1.07-2.62; P = 0.02) than patients with high expression. MiR-451 was an independent prognostic factor in NPC in multivariate Cox regression analysis. Ectopic expression of miR-451 suppressed cell viability, colony formation, and cell migration and invasion in vitro, and inhibited xenograft tumor growth in vivo. MIF was verified as a direct target of miR-451, and MIF regulated NPC cell growth and invasion. CONCLUSIONS: The newly identified miR-451/MIF pathway provides insight into NPC initiation and progression, and may represent a novel therapeutic target. |
format | Online Article Text |
id | pubmed-3853142 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-38531422013-12-07 MiR-451 inhibits cell growth and invasion by targeting MIF and is associated with survival in nasopharyngeal carcinoma Liu, Na Jiang, Ning Guo, Rui Jiang, Wei He, Qing-Mei Xu, Ya-Fei Li, Ying-Qin Tang, Ling-Long Mao, Yan-Ping Sun, Ying Ma, Jun Mol Cancer Research BACKGROUND: MiRNAs play important roles in diverse biological processes including tumorigenesis. However, little is known about the function and mechanism of miR-451 in nasopharyngeal carcinoma (NPC). METHODS: Quantitative RT-PCR was used to quantify miR-451 expression in NPC cell lines and clinical tissues. Kaplan-Meier curves were used to estimate the association between miR-451 expression and survival. The MTT, colony formation, Transwell migration and invasion assays, and a xenograft model were performed. A miR-451 target was confirmed using luciferase reporter assays, quantitative RT-PCR, and Western blotting. RESULTS: MiR-451 was significantly downregulated in NPC cell lines and clinical tissues (P < 0.01). Patients with low expression of miR-451 had poorer overall survival (HR, 1.98; 95% CI, 1.16-3.34; P = 0.01) and disease-free survival (HR, 1.68; 95% CI, 1.07-2.62; P = 0.02) than patients with high expression. MiR-451 was an independent prognostic factor in NPC in multivariate Cox regression analysis. Ectopic expression of miR-451 suppressed cell viability, colony formation, and cell migration and invasion in vitro, and inhibited xenograft tumor growth in vivo. MIF was verified as a direct target of miR-451, and MIF regulated NPC cell growth and invasion. CONCLUSIONS: The newly identified miR-451/MIF pathway provides insight into NPC initiation and progression, and may represent a novel therapeutic target. BioMed Central 2013-10-20 /pmc/articles/PMC3853142/ /pubmed/24138931 http://dx.doi.org/10.1186/1476-4598-12-123 Text en Copyright © 2013 Liu et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Liu, Na Jiang, Ning Guo, Rui Jiang, Wei He, Qing-Mei Xu, Ya-Fei Li, Ying-Qin Tang, Ling-Long Mao, Yan-Ping Sun, Ying Ma, Jun MiR-451 inhibits cell growth and invasion by targeting MIF and is associated with survival in nasopharyngeal carcinoma |
title | MiR-451 inhibits cell growth and invasion by targeting MIF and is associated with survival in nasopharyngeal carcinoma |
title_full | MiR-451 inhibits cell growth and invasion by targeting MIF and is associated with survival in nasopharyngeal carcinoma |
title_fullStr | MiR-451 inhibits cell growth and invasion by targeting MIF and is associated with survival in nasopharyngeal carcinoma |
title_full_unstemmed | MiR-451 inhibits cell growth and invasion by targeting MIF and is associated with survival in nasopharyngeal carcinoma |
title_short | MiR-451 inhibits cell growth and invasion by targeting MIF and is associated with survival in nasopharyngeal carcinoma |
title_sort | mir-451 inhibits cell growth and invasion by targeting mif and is associated with survival in nasopharyngeal carcinoma |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3853142/ https://www.ncbi.nlm.nih.gov/pubmed/24138931 http://dx.doi.org/10.1186/1476-4598-12-123 |
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