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Long noncoding RNA SNHG6 promotes the progression of colorectal cancer through sponging miR-760 and activation of FOXC1

Authors Zhu Y, Xing Y, Chi F, Sun W, Zhang Z, Piao D

Received 5 April 2018

Accepted for publication 26 May 2018

Published 12 September 2018 Volume 2018:11 Pages 5743—5752

DOI https://doi.org/10.2147/OTT.S170246

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Andrew Yee

Peer reviewer comments 3

Editor who approved publication: Dr Samir Farghaly


Yuekun Zhu,1,* Yanwei Xing,1,* Fengxu Chi,1 Weidong Sun,1 Zhiyong Zhang,2 Daxun Piao1

1Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China; 2Department of Surgery, Robert-Wood-Johnson Medical School University Hospital, Rutgers University, The State University of New Jersey, New Brunswick, NJ, USA

*These authors contributed equally to this work

Background: Colorectal cancer (CRC) is one of most common cancers worldwide. Long non-coding RNA SNHG6 has been reported to act as essential regulators in several cancers. However, the functional role and molecular mechanism of SNHG6 in colorectal cancer remain unclear.
Methods: Quantitative real-time polymerase chain reaction (PCR) was performed to evaluate the SNHG6 expression in CRC tissues. Colony formation, transwell assays and in vivo mice models were carried out to assess the effect of SNHG6 on CRC biological functions.
Results: In the present study, we showed that the expression of SNHG6 was significantly upregulated in CRC tissues and cell lines. High expression of SNHG6 was associated with shorter overall survival in CRC patients. Functionally, SNHG6 knockdown significantly inhibited cell proliferation, invasion and migration both in vitro and in vivo. Mechanically, miR-760 was a direct target of SNHG6, and repression of miR-760 could rescue the inhibitory effect of SNHG6 knockdown on CRC progression. In addition, SNHG6 positively regulated FOXC1 expression through sponging miR-760 in CRC cells, thus indicating that SNHG6 exerted an oncogenic role in CRC by acting as a ceRNA of miR-760.
Conclusion: Our results indicate that long non-coding RNA SNHG6 promotes colorectal cancer progression by sequestering miR-760 and activating FOXC1, our findings suggest that SNHG6 may serve as a potential therapeutic target for CRC.

Keywords: lncRNA SNHG6, miR-760, FOXC1, colorectal cancer

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