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Upregulation of MiR-196a promotes cell proliferation by downregulating p27(kip1) in laryngeal cancer
BACKGROUND: Accumulating evidence has confirmed that miR-196a plays a critical role in tumorigenesis and tumor progression in a variety of cancers. It has been demonstrated that miR-196a is highly up-regulated in laryngeal cancer by miRNA profiling analysis. However, the functional mechanism of miR-...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5039793/ https://www.ncbi.nlm.nih.gov/pubmed/27678369 http://dx.doi.org/10.1186/s40659-016-0100-9 |
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author | Jin, Cheng Zhang, Yi Li, Jiping |
author_facet | Jin, Cheng Zhang, Yi Li, Jiping |
author_sort | Jin, Cheng |
collection | PubMed |
description | BACKGROUND: Accumulating evidence has confirmed that miR-196a plays a critical role in tumorigenesis and tumor progression in a variety of cancers. It has been demonstrated that miR-196a is highly up-regulated in laryngeal cancer by miRNA profiling analysis. However, the functional mechanism of miR-196a in laryngeal cancer remains unclear. This study aims to explore the mechanism of miR-196a in laryngeal cancer. METHODS: In the present study, we conducted qPCR analysis of miR-196a expression in human laryngeal cancer and showed that miR-196a was overexpressed in tumor-derived samples and laryngeal cancer cell lines compared with matched normal controls. Further functional analysis of miR-196a demonstrated that the inhibition of miR-196a could inhibit laryngeal cell-cycle progression and proliferation in vitro. Luciferase reporter assay and western blot confirmed that miR-196a directly targeted p27kip1. Moreover, in order to investigate whether miR-196a regulated cell growth in laryngeal cancer cells by targeting p27kip1, rescue studies were performed in laryngeal cancer cells. RESULTS: Results showed that overexpression of p27kip1 rescue decreased cell proliferation caused by miR-196a inhibitors. A negative relation between miR-196a and p27kip1 expression in laryngeal cancer tissues were also noted by further analyses. CONCLUSIONS: The present study showed that miR-196a was upregulated in laryngeal cancer and promoted cell proliferation by downregulating p27kip1 in laryngeal cancer. However, further studies are needed to verify this finding. |
format | Online Article Text |
id | pubmed-5039793 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-50397932016-10-05 Upregulation of MiR-196a promotes cell proliferation by downregulating p27(kip1) in laryngeal cancer Jin, Cheng Zhang, Yi Li, Jiping Biol Res Research Article BACKGROUND: Accumulating evidence has confirmed that miR-196a plays a critical role in tumorigenesis and tumor progression in a variety of cancers. It has been demonstrated that miR-196a is highly up-regulated in laryngeal cancer by miRNA profiling analysis. However, the functional mechanism of miR-196a in laryngeal cancer remains unclear. This study aims to explore the mechanism of miR-196a in laryngeal cancer. METHODS: In the present study, we conducted qPCR analysis of miR-196a expression in human laryngeal cancer and showed that miR-196a was overexpressed in tumor-derived samples and laryngeal cancer cell lines compared with matched normal controls. Further functional analysis of miR-196a demonstrated that the inhibition of miR-196a could inhibit laryngeal cell-cycle progression and proliferation in vitro. Luciferase reporter assay and western blot confirmed that miR-196a directly targeted p27kip1. Moreover, in order to investigate whether miR-196a regulated cell growth in laryngeal cancer cells by targeting p27kip1, rescue studies were performed in laryngeal cancer cells. RESULTS: Results showed that overexpression of p27kip1 rescue decreased cell proliferation caused by miR-196a inhibitors. A negative relation between miR-196a and p27kip1 expression in laryngeal cancer tissues were also noted by further analyses. CONCLUSIONS: The present study showed that miR-196a was upregulated in laryngeal cancer and promoted cell proliferation by downregulating p27kip1 in laryngeal cancer. However, further studies are needed to verify this finding. BioMed Central 2016-09-27 /pmc/articles/PMC5039793/ /pubmed/27678369 http://dx.doi.org/10.1186/s40659-016-0100-9 Text en © The Author(s) 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Jin, Cheng Zhang, Yi Li, Jiping Upregulation of MiR-196a promotes cell proliferation by downregulating p27(kip1) in laryngeal cancer |
title | Upregulation of MiR-196a promotes cell proliferation by downregulating p27(kip1) in laryngeal cancer |
title_full | Upregulation of MiR-196a promotes cell proliferation by downregulating p27(kip1) in laryngeal cancer |
title_fullStr | Upregulation of MiR-196a promotes cell proliferation by downregulating p27(kip1) in laryngeal cancer |
title_full_unstemmed | Upregulation of MiR-196a promotes cell proliferation by downregulating p27(kip1) in laryngeal cancer |
title_short | Upregulation of MiR-196a promotes cell proliferation by downregulating p27(kip1) in laryngeal cancer |
title_sort | upregulation of mir-196a promotes cell proliferation by downregulating p27(kip1) in laryngeal cancer |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5039793/ https://www.ncbi.nlm.nih.gov/pubmed/27678369 http://dx.doi.org/10.1186/s40659-016-0100-9 |
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