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Long Non-Coding RNA LINC00511 Mediates the Effects of ESR1 on Proliferation and Invasion of Ovarian Cancer Through miR-424-5p and miR-370-5p

Authors Wang K, Zhu G, Bao S, Chen S

Received 23 September 2019

Accepted for publication 23 November 2019

Published 27 December 2019 Volume 2019:11 Pages 10807—10819

DOI https://doi.org/10.2147/CMAR.S232140

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Chien-Feng Li


Kang Wang,1,2 Genhai Zhu,2 Shan Bao,2 Shiling Chen1

1Department of Gynecology and Obstetrics, Center for Reproductive Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, People’s Republic of China; 2Department of Gynecology, Hainan General Hospital, Haikou, Hainan 570000, People’s Republic of China

Correspondence: Shiling Chen
Department of Gynecology and Obstetrics, Center for Reproductive Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, People’s Republic of China
Email chen_shiling2019@163.com

Introduction: Estrogen receptor 1 (ESR1) plays an important role in the pathological events of ovarian cancer (OV), but the underlying mechanism is not completely understood. Using bioinformatics analysis, we found that ESR1 is involved in the regulation of some lncRNAs that are highly expressed in ovarian cancer. The lncRNAs might mediate the roles of ESR1 in OV occurrence and progression.
Methods: This study measured the expression of the lncRNAs in OV cell lines using qRT-PCR. Some of the lncRNAs were silenced or overexpressed to determine their effects on the growth and invasion of CAOV3 cells with the stimulation of 17 beta-estradiol or not.
Results: ESR1-expressing OV cells (CAOV3 cells) shows higher LINC00511 and RP11-166P13.3 expression than the ESR1-losing OV cells (UWB1.289 cells). Depletion of the two lncRNAs enhanced cell viability and invasion and decreased apoptosis rate. In these respects, effects of LINC00511 were more remarkable than that those of RP11-166P13.3. Treatment with 17 beta-estradiol to stimulate ESR1 increased LINC00511 expression, while ESR1 inhibitor Fulvestrant decreased LINC00511 expression. FISH assay confirmed that LINC00511 is present in the cytoplasm and nucleus. Bioinformatics analysis revealed the interaction of LINC00511 with miR-424-5p and miR-370-5p, which was further identified by RNA-pull down assay. As indicated by RIP assay, silencing LINC00511 increased the interaction between Ago protein and these two miRNAs.
Discussion: Our study showed that ESR1-induced upregulation of LINC00511 promoted proliferation and invasion of CAOV3 cells probably through sponging miR-424-5p and miR-370-5p.

Keywords: ESR1, long non-coding RNA LINC00511, progression, ovarian cancer

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