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Cancer Cell International
Published in: Cancer Cell International 1/2018

Open Access 01-12-2018 | Primary research

MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3

Authors: Yong-Xia Wang, Hui-Fang Zhu, Zhe-Ying Zhang, Feng Ren, Yu-Han Hu

Published in: Cancer Cell International | Issue 1/2018

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Abstract

Background

Growing evidence suggests that MiRNAs play essential roles in the initiation and progression of colorectal cancer (CRC). The aberrant expression of miR-384 has been reported in some cancers. However, the role and mechanism of miR-384 in CRC proliferation remains unknown.

Methods

The expression of miR-384 was detected in CRC and their paired normal tissues by real-time PCR. In vivo and in vitro assays were conducted to confirm the role of miR-384 in the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro assays were used to confirm that AKT3 was the target gene of miR-384. Finally, Spearman’s correlation analyses was carried out to analyze the relationship between miR-384 expression and AKT3 expression in CRC.

Results

MiR-384 was down‑regulated in CRC tissues. The in vivo and vitro functional assays verified that the ectopic upregulation of miR-384 inhibited the proliferation of CRC and the inhibition of miR-384 promoted the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro functional assays confirmed AKT3 as the target gene of miR-384. The expression of miR-384 was negatively correlated with the expressions of AKT3.

Conclusion

Our study verified that miR-384 could significantly suppress the proliferation of CRC by directing targeting AKT3.
Appendix
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Metadata
Title
MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3
Authors
Yong-Xia Wang
Hui-Fang Zhu
Zhe-Ying Zhang
Feng Ren
Yu-Han Hu
Publication date
01-12-2018
Publisher
BioMed Central
Published in
Cancer Cell International / Issue 1/2018
Electronic ISSN: 1475-2867
DOI
https://doi.org/10.1186/s12935-018-0628-6

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