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miR-320b suppresses cell proliferation by targeting c-Myc in human colorectal cancer cells

BACKGROUND: MicroRNAs (miRNAs) are small noncoding RNAs that potentially play a critical role in tumorigenesis. Mounting evidence indicates that one specific miRNA: miR-320b is down regulated in numerous human cancers, including colorectal cancer (CRC); making the hypothesis that miR-320b may play a...

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Autores principales: Wang, Hantao, Cao, Fuao, Li, Xu, Miao, Hua, E, Jifu, Xing, Junjie, Fu, Chuan-gang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4617986/
https://www.ncbi.nlm.nih.gov/pubmed/26487644
http://dx.doi.org/10.1186/s12885-015-1728-5
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author Wang, Hantao
Cao, Fuao
Li, Xu
Miao, Hua
E, Jifu
Xing, Junjie
Fu, Chuan-gang
author_facet Wang, Hantao
Cao, Fuao
Li, Xu
Miao, Hua
E, Jifu
Xing, Junjie
Fu, Chuan-gang
author_sort Wang, Hantao
collection PubMed
description BACKGROUND: MicroRNAs (miRNAs) are small noncoding RNAs that potentially play a critical role in tumorigenesis. Mounting evidence indicates that one specific miRNA: miR-320b is down regulated in numerous human cancers, including colorectal cancer (CRC); making the hypothesis that miR-320b may play a key role in tumorigenesis plausible. However, its role in carcinogenesis remains poorly defined. The goal of this study is to better clarify the role of miR-320b in tumor growth of CRC. METHODS: Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was conducted to detect the expression of miR-320b in CRC tissues and 5 CRC cell lines. The effect of miR-320b on cell proliferation was analyzed in vitro and in vivo. Furthermore, a luciferase reporter assay was performed to measure the target effects of miR-320b. Lastly, the messenger RNA (mRNA) and protein levels of the gene c-MYC were measured in CRC cell lines and tissues by qRT-PCR, and confirmed via Western blot and Immunohistochemical (IHC) staining. RESULTS: The results presented here showed that miR-320b expression was down regulated in both CRC tissues and cells. Overexpression of miR-320b in CRC cells was statistically correlated with a decrease of cell growth in vitro and in vivo, while c-MYC was identified as a target gene of miR-320b in CRC. Furthermore, it was found that up-regulation of c-Myc can attenuate the effects induced by miR-320b. CONCLUSIONS: Our identification of c-MYC as a target gene of miR-320b provides new insights into the pathophysiology of CRC proliferation, and identifies miR-320b as a novel therapeutic target for the treatment of CRC.
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spelling pubmed-46179862015-10-25 miR-320b suppresses cell proliferation by targeting c-Myc in human colorectal cancer cells Wang, Hantao Cao, Fuao Li, Xu Miao, Hua E, Jifu Xing, Junjie Fu, Chuan-gang BMC Cancer Research Article BACKGROUND: MicroRNAs (miRNAs) are small noncoding RNAs that potentially play a critical role in tumorigenesis. Mounting evidence indicates that one specific miRNA: miR-320b is down regulated in numerous human cancers, including colorectal cancer (CRC); making the hypothesis that miR-320b may play a key role in tumorigenesis plausible. However, its role in carcinogenesis remains poorly defined. The goal of this study is to better clarify the role of miR-320b in tumor growth of CRC. METHODS: Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was conducted to detect the expression of miR-320b in CRC tissues and 5 CRC cell lines. The effect of miR-320b on cell proliferation was analyzed in vitro and in vivo. Furthermore, a luciferase reporter assay was performed to measure the target effects of miR-320b. Lastly, the messenger RNA (mRNA) and protein levels of the gene c-MYC were measured in CRC cell lines and tissues by qRT-PCR, and confirmed via Western blot and Immunohistochemical (IHC) staining. RESULTS: The results presented here showed that miR-320b expression was down regulated in both CRC tissues and cells. Overexpression of miR-320b in CRC cells was statistically correlated with a decrease of cell growth in vitro and in vivo, while c-MYC was identified as a target gene of miR-320b in CRC. Furthermore, it was found that up-regulation of c-Myc can attenuate the effects induced by miR-320b. CONCLUSIONS: Our identification of c-MYC as a target gene of miR-320b provides new insights into the pathophysiology of CRC proliferation, and identifies miR-320b as a novel therapeutic target for the treatment of CRC. BioMed Central 2015-10-20 /pmc/articles/PMC4617986/ /pubmed/26487644 http://dx.doi.org/10.1186/s12885-015-1728-5 Text en © Wang et al. 2015 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
Wang, Hantao
Cao, Fuao
Li, Xu
Miao, Hua
E, Jifu
Xing, Junjie
Fu, Chuan-gang
miR-320b suppresses cell proliferation by targeting c-Myc in human colorectal cancer cells
title miR-320b suppresses cell proliferation by targeting c-Myc in human colorectal cancer cells
title_full miR-320b suppresses cell proliferation by targeting c-Myc in human colorectal cancer cells
title_fullStr miR-320b suppresses cell proliferation by targeting c-Myc in human colorectal cancer cells
title_full_unstemmed miR-320b suppresses cell proliferation by targeting c-Myc in human colorectal cancer cells
title_short miR-320b suppresses cell proliferation by targeting c-Myc in human colorectal cancer cells
title_sort mir-320b suppresses cell proliferation by targeting c-myc in human colorectal cancer cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4617986/
https://www.ncbi.nlm.nih.gov/pubmed/26487644
http://dx.doi.org/10.1186/s12885-015-1728-5
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