Abstract

Long noncoding RNAs (lncRNAs) have recently emerged as pivotal regulators in governing fundamental biological processes, as well as in tumorigenesis. The nuclear paraspeckle assembly transcript 1 (NEAT1) is one of the most highly regulated lncRNAs in recent genomic datasets, however, its biological role and regulatory mechanism in ovarian cancer (OC) development and progression are poorly defined. In this study, we identified that NEAT1 was up‐regulated in OC patients and cell lines, and its expression was associated with the FIGO stage and lymph node metastasis. Furthermore, the ectopic expression of NEAT1_1 in OVCAR‐3 cell lines promoted cell proliferation and invasion, whereas knockdown of NEAT1_1 did the opposite. Furthermore, NEAT1_1 was stabilized by an RNA‐binding protein HuR, but suppressed by miR‐124‐3p in OC cells. Accordingly, the increased HuR mRNA and decreased miR‐124‐3p levels were observed in OC patients. These results suggested that lncRNA NEAT1, whose expression was collaboratively controlled by HuR and miR‐124‐3p, could regulate ovarian carcinogenesis and may serve as a potential target for antineoplastic therapies.

Highlights

  • Ovarian cancer (OC) is the most lethal gynecological cancer and a common cause of cancer-­related deaths in women worldwide [1, 2]

  • Metastasis-­associated lung adenocarcinoma transcript 1 (MALAT1), named nuclear-­enriched abundant transcript 2 (NEAT2), is a widely expressed Long noncoding RNAs (lncRNAs) that was first identified as a factor indicating high metastatic potential and poor prognosis in non-s­mall-­ cell lung cancer (NSCLC) [11,12,13,14]

  • We further identified that the up-r­ egulation of nuclear paraspeckle assembly transcript 1 (NEAT1) in OC was mediated by HuR, which binds to NEAT1 and increases the steady-­state levels of NEAT1

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Summary

Introduction

Ovarian cancer (OC) is the most lethal gynecological cancer and a common cause of cancer-­related deaths in women worldwide [1, 2]. A deep understanding of the molecular mechanisms implicated in ovarian carcinogenesis is required for the development of OC prevention, diagnosis, and therapy. Recent studies have revealed that a number of lncRNAs have essential roles in a diverse range of cellular processes such as proliferation, differentiation, apoptosis, and cell fate as well as disease pathogenesis, causing a paradigm change in our understanding of gene regulation networks [3,4,5]. Expressed gene 3 (MEG3) encodes an lncRNA, which is lost or significantly reduced in neuroblastomas, hepatocellular cancers, gastric cancer, and gliomas [17, 18]. Identification of differential expression is the first step in the elucidation of lncRNA-­ based molecular mechanisms capable of regulating tumorigenesis

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