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Knockdown of long noncoding RNA 00152 (LINC00152) inhibits human retinoblastoma progression

Authors Li S, Wen D, Che S, Cui Z, Sun Y, Ren H, Hao J

Received 20 December 2017

Accepted for publication 12 March 2018

Published 6 June 2018 Volume 2018:11 Pages 3215—3223

DOI https://doi.org/10.2147/OTT.S160428

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Ms Justinn Cochran

Peer reviewer comments 3

Editor who approved publication: Dr Ingrid Espinoza


Songhe Li,1 Dacheng Wen,2 Songtian Che,3 Zhihua Cui,1 Yabin Sun,1 Hua Ren,1 Jilong Hao1

1Department of Ophthalmology, The First Hospital of Jilin University, Changchun, People’s Republic of China; 2Department of Gastrointestinal Nutrition and Hernia Surgery, The Second Hospital of Jilin University, Changchun, People’s Republic of China; 3Department of Ophthalmology, The Second Hospital of Jilin University, Changchun, People’s Republic of China

Background: A growing body of evidence supports the involvement of long noncoding RNA 00152 (LINC00152) in the progression and metastasis of multiple cancers. However, the exact roles of LINC00152 in the progression of human retinoblastoma (RB) remain unknown. We explored the expression and biological function of human RB.
Materials and methods: The expression level of LINC00152 in RB tissues and cells was analyzed using quantitative real-time PCR. The function of LINC00152 was determined using a series of in vitro assays. In vivo, a nude mouse model was established to analyze the function of LINC00152. Gene and protein expressions were detected using quantitative real-time PCR and Western blot assays, respectively.
Results: The expression of LINC00152 mRNA was upregulated in RB tissues and cell lines. Knockdown of LINC00152 significantly inhibited cell proliferation, colony formation, migration, and invasion and promoted cell apoptosis and caspase-3 and caspase-8 activities in vitro, as well as suppressing tumorigenesis in vivo. We identified several genes related to proliferation, apoptosis, and invasion including Ki-67, Bcl-2, and MMP-9 that were transcriptionally inactivated by LINC00152.
Conclusion: Taken together, these data implicate LINC00152 as a therapeutic target in RB.

Keywords: retinoblastoma, LINC00152, proliferation, invasion

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