miR-320b suppresses cell proliferation by targeting c-Myc in human colorectal cancer cellsReportar como inadecuado

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BMC Cancer

, 15:748

First Online: 20 October 2015Received: 24 December 2014Accepted: 08 October 2015DOI: 10.1186-s12885-015-1728-5

Cite this article as: Wang, H., Cao, F., Li, X. et al. BMC Cancer 2015 15: 748. doi:10.1186-s12885-015-1728-5


BackgroundMicroRNAs 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.

MethodsQuantitative 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.

ResultsThe 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.

ConclusionsOur 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.

KeywordsColorectal cancer CRC miR-320b c-Myc Cyclin D1 AbbreviationCRCColorectal cancer

mRNAMessenger RNA

qRT-PCRQuantitative real-time PCR



CLASHCrosslinking, ligation, and sequencing of hybrids

Hantao Wang, Fuao Cao and Xu Li contributed equally to this work.

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Autor: Hantao Wang - Fuao Cao - Xu Li - Hua Miao - Jifu E - Junjie Xing - Chuan-gang Fu

Fuente: https://link.springer.com/

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