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Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV
BACKGROUND: microRNAs are small noncoding RNAs that modulate a variety of cellular processes by regulating multiple targets, which can promote or inhibit the development of malignant behaviors. Accumulating evidence suggests miR-24 plays important roles in human carcinogenesis. However, its precise...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4041902/ https://www.ncbi.nlm.nih.gov/pubmed/24886316 http://dx.doi.org/10.1186/1476-4598-13-127 |
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author | Duan, Yantao Hu, Lei Liu, Bing Yu, Beiqin Li, Jianfang Yan, Min Yu, Yingyan Li, Chen Su, Liping Zhu, Zhenggang Xiang, Ming Liu, Bingya Yang, Qiumeng |
author_facet | Duan, Yantao Hu, Lei Liu, Bing Yu, Beiqin Li, Jianfang Yan, Min Yu, Yingyan Li, Chen Su, Liping Zhu, Zhenggang Xiang, Ming Liu, Bingya Yang, Qiumeng |
author_sort | Duan, Yantao |
collection | PubMed |
description | BACKGROUND: microRNAs are small noncoding RNAs that modulate a variety of cellular processes by regulating multiple targets, which can promote or inhibit the development of malignant behaviors. Accumulating evidence suggests miR-24 plays important roles in human carcinogenesis. However, its precise biological role remains largely elusive. This study examined the role of miR-24 in gastric cancer (GC). METHODS: The expression of miR-24 in GC tissues compared with matched non-tumor tissues and GC cells was detected by qRT-PCR. Synthetic short single or double stranded RNA oligonucleotides and lentiviral vectors were used to regulate miR-24 expression in GC cells to investigate its function in vitro and in vivo. RESULTS: miR-24 was significantly downregulated in GC tissues compared with matched non-tumor tissues and was associated with tumor differentiation. Ectopic expression of miR-24 in SGC-7901 GC cells suppressed cell proliferation, migration and invasion in vitro as well as tumorigenicity in vivo by inducing cell cycle arrest in G0/G1 phase and promoting cell apoptosis. Furthermore, we identified RegIV as a target of miR-24 and demonstrated that miR-24 regulated RegIV expression via binding its 3′ untranslated region. CONCLUSIONS: miR-24 functions as a novel tumor suppressor in GC and the anti-oncogenic activity may involve its inhibition of the target gene RegIV. These findings suggest the possibility for miR-24 as a therapeutic target in GC. |
format | Online Article Text |
id | pubmed-4041902 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-40419022014-06-04 Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV Duan, Yantao Hu, Lei Liu, Bing Yu, Beiqin Li, Jianfang Yan, Min Yu, Yingyan Li, Chen Su, Liping Zhu, Zhenggang Xiang, Ming Liu, Bingya Yang, Qiumeng Mol Cancer Research BACKGROUND: microRNAs are small noncoding RNAs that modulate a variety of cellular processes by regulating multiple targets, which can promote or inhibit the development of malignant behaviors. Accumulating evidence suggests miR-24 plays important roles in human carcinogenesis. However, its precise biological role remains largely elusive. This study examined the role of miR-24 in gastric cancer (GC). METHODS: The expression of miR-24 in GC tissues compared with matched non-tumor tissues and GC cells was detected by qRT-PCR. Synthetic short single or double stranded RNA oligonucleotides and lentiviral vectors were used to regulate miR-24 expression in GC cells to investigate its function in vitro and in vivo. RESULTS: miR-24 was significantly downregulated in GC tissues compared with matched non-tumor tissues and was associated with tumor differentiation. Ectopic expression of miR-24 in SGC-7901 GC cells suppressed cell proliferation, migration and invasion in vitro as well as tumorigenicity in vivo by inducing cell cycle arrest in G0/G1 phase and promoting cell apoptosis. Furthermore, we identified RegIV as a target of miR-24 and demonstrated that miR-24 regulated RegIV expression via binding its 3′ untranslated region. CONCLUSIONS: miR-24 functions as a novel tumor suppressor in GC and the anti-oncogenic activity may involve its inhibition of the target gene RegIV. These findings suggest the possibility for miR-24 as a therapeutic target in GC. BioMed Central 2014-05-28 /pmc/articles/PMC4041902/ /pubmed/24886316 http://dx.doi.org/10.1186/1476-4598-13-127 Text en Copyright © 2014 Duan 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 credited. 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 Duan, Yantao Hu, Lei Liu, Bing Yu, Beiqin Li, Jianfang Yan, Min Yu, Yingyan Li, Chen Su, Liping Zhu, Zhenggang Xiang, Ming Liu, Bingya Yang, Qiumeng Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV |
title | Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV |
title_full | Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV |
title_fullStr | Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV |
title_full_unstemmed | Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV |
title_short | Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV |
title_sort | tumor suppressor mir-24 restrains gastric cancer progression by downregulating regiv |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4041902/ https://www.ncbi.nlm.nih.gov/pubmed/24886316 http://dx.doi.org/10.1186/1476-4598-13-127 |
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