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Long Noncoding RNA DIO3OS Hinders Cell Malignant Behaviors of Hepatocellular Carcinoma Cells Through the microRNA-328/Hhip Axis

Authors Wang Z, Song L, Ye Y, Li W

Received 14 January 2020

Accepted for publication 30 April 2020

Published 25 May 2020 Volume 2020:12 Pages 3903—3914

DOI https://doi.org/10.2147/CMAR.S245990

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Professor Bilikere Dwarakanath


Zhanpeng Wang,1 Lina Song,2 Yanshuo Ye,1 Wei Li1

1Department of Hepatobiliary-Pancreatic Surgery, China-Japan Union Hospital of Jilin University, Changchun 130000, People’s Republic of China; 2Department of Laboratory Medicine Center, China-Japan Union Hospital of Jilin University, Changchun 130000, People’s Republic of China

Correspondence: Wei Li
Department of Hepatobiliary-Pancreatic Surgery, China-Japan Union Hospital of Jilin University, No. 126 Xiantai Street, Changchun 130000, People’s Republic of China
Tel/ Fax +86-431-89876756
Email Liwei12162@163.com

Background: The decline of a long non-coding RNA (lncRNA) DIO3OS was implicated in a plethora of cancers, while the relevance in hepatocellular carcinoma (HCC) has not been mentioned. Accordingly, we set to determine the functional role of DIO3OS and the molecular mechanism in HCC progression.
Materials and Methods: The differentially expressed lncRNAs, mRNAs, and microRNAs (miRNAs) were obtained through the datasets GSE101728 and GES57555. Afterwards, DIO3OS was enhanced in HCC cells to examine the behavior changes. Subcellular localization of DIO3OS was determined through website prediction and experimental validation. The expression of Hedgehog (Hh) signaling pathway-related genes was detected. The effects of DIO3OS overexpression on tumor growth were evaluated as well.
Results: DIO3OS was lower in HCC tissues and cells, while upregulation of DIO3OS repressed malignant biological behavior both in vitro and in vivo. DIO3OS, localized in the cytoplasm, inhibited the occurrence of HCC by disrupting the Hh pathway by sponging miR-328 to mediate Hh interacting protein (Hhip).
Conclusion: All in all, the obtained data suggested that DIO3OS interacted with Hhip-dependent Hh signaling pathway to inhibit HCC progression through binding to miR-328, which may be a potent therapeutic target for HCC.

Keywords: hepatocellular carcinoma, DIO3OS, competing endogenous RNA, microRNA-328, Hhip, hedgehog signaling pathway

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