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LINC00339 promotes growth and invasiveness of hepatocellular carcinoma by the miR-1182/SKA1 pathway

Authors Xiao J, Yu H, Ma Z

Received 2 March 2019

Accepted for publication 1 May 2019

Published 6 June 2019 Volume 2019:12 Pages 4481—4488

DOI https://doi.org/10.2147/OTT.S207397

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Jyoti Bajaj

Peer reviewer comments 2

Editor who approved publication: Dr Yao Dai


Jun Xiao, Haibo Yu, Zhongwu Ma

Department of Hepatobiliary Surgery, Wenzhou Central Hospital, Wenzhou 325000, People’s Republic of China

Background: Extensive research has shown that long noncoding RNA (lncRNA) is involved in tumorigenesis, including hepatocellular carcinoma (HCC). The lncRNA LINC00339 was reported to regulate the development of lung cancer or breast cancer. However, whether LINC00339 participates in HCC progression remains unclear. Here, our results showed that LINC00339 was upregulated in HCC.
Methods: qRT-PCR and in situ hybridization (ISH) was used to analyze LINC00339 expression in tumor tissues and cell lines. CCK8 and colony formation assays were used to analyze cell proliferation. Transwell assay was used to analyze cell migration and invasion. Xenograft experiment was used to test tumor growth in vivo.
Results: LINC00339 overexpression was correlated with an advanced stage, metastasis, and bad prognosis in HCC patients. Functional investigation showed that LINC00339 knockdown significantly suppressed HCC cell proliferation, migration, and invasion. Moreover, decreased LINC00339 expression inhibited HCC growth in vivo. Mechanistically, LINC00339 could interact with miR-1182 to promote SKA1 expression. We also demonstrated that SKA1 acted as an oncogene and SKA1 upregulation reversed the effect of LINC00339 silencing.
Conclusion: Our results illustrated that the LINC00339/miR-1182/SKA1 axis plays an essential role in HCC progression.

Keywords: LINC00339, miR-1182, SKA1, hepatocellular carcinoma, progression
 

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