Back to Journals » OncoTargets and Therapy » Volume 11

Overexpressing lncRNA SNHG16 inhibited HCC proliferation and chemoresistance by functionally sponging hsa-miR-93

Authors Xu F, Zha G, Wu Y, Cai W, Ao J

Received 31 July 2018

Accepted for publication 31 August 2018

Published 7 December 2018 Volume 2018:11 Pages 8855—8863

DOI https://doi.org/10.2147/OTT.S182005

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 3

Editor who approved publication: Dr Takuya Aoki


Fengfeng Xu,1 Guoqing Zha,2 Yanpeng Wu,1 Weilong Cai,1 Jian Ao1

1Department of General Surgery, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, People’s Republic of China; 2The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, People’s Republic of China

Background: Long noncoding RNAs (lncRNAs) have been identified as prognostic biomarkers and functional regulators in human cancers. The present study aimed to determine the expressions and functions of an lncRNA, Small Nucleolar RNA Host Gene 16 (SNHG16), in hepatocellular carcinoma (HCC).
Patients and methods: SNHG16 expressions were tested by quantitative real-time PCR (qRT-PCR) in HCC cell lines, as well as 43 pairs of HCC tissues and pair-matched healthy hepatic tissues. It was overexpressed in Hep3B and HuH7 cells. The effects of SNHG16 overexpression in HCC in vitro proliferation, 5-fluorouracil (5-FU) chemoresistance, and in vivo tumor growth were tested. A potential microRNA (miRNA) sponge target of SNHG16, hsa-miR-93, was tested by luciferase reporter assay and qRT-PCR. In addition, hsa-miR-93 was upregulated in SNHG16-overexpressed HCC cells to examine its effect on SNHG16-mediated cancer cell functional regulation in HCC.
Results: SNHG16 levels were markedly downregulated in both HCC cell lines and HCC tissues. Lentivirus-mediated SNHG16 overexpression inhibited HCC cell proliferation, 5-FU chemoresistance, and in vivo tumor growth. Hsa-miR-93 was confirmed to be directly sponging on SNHG16. Its upregulation in HCC cells reversed SNHG16 overexpression and induced tumor-suppressing effects in HCC cells.
Conclusion: Our data demonstrate that SNHG16 plays a critical role in HCC development via functionally sponging hsa-miR-93.

Keywords: lncRNA, SNHG16, miRNA, hsa-miR-93, proliferation

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]