Abstract

BackgroundPrevious literature has revealed long non-coding RNAs (lncRNAs) are crucial regulators for cell functions and gene expression. LncRNA fetal-lethal non-coding developmental regulatory RNA (FENDRR) was reported as a biological suppressor in several types of human cancers, yet relevant mechanisms and biological effects of FENDRR with regards to cervical cancer (CC) are not explored until now.MethodsIn this study, quantitative real-time polymerase chain reaction (qRT-PCR) analysis detected gene expression in tissues and cells. Gain- or loss-of-function experiments revealed the biological effects of FENDRR and miR-15a/b-5p on CC cell functions. Bioinformatics tools were used to predict the relevant genes. Mechanism experiments including RNA immunoprecipitation (RIP) assay, pull down assay and luciferase reporter assay depicted the binding situation and coexistence of indicated genes.ResultsFENDRR was downregulated in CC tissues and cells, which suppressed CC progression. MiR-15a-5p and miR-15b-5p shared binding sites with FENDRR and had interaction with FENDRR. Tubulin alpha1A (TUBA1A) was downregulated in CC tissues and positively modulated by FENDRR. TUBA1A was the target of miR-15a/b-5p. TUBA1A silencing rescued the effect of FENDRR overexpression on CC cell growth and migration.ConclusionFENDRR inhibits CC progression through upregulating TUBA1A in a miR-15a/b-5p-dependent manner.

Highlights

  • Previous literature has revealed long non-coding RNAs are crucial regulators for cell functions and gene expression

  • fetal-lethal non-coding developmental regulatory RNA (FENDRR) inhibits CC progression in vitro and vivo In our study, we first detected relative FENDRR expression in CC tissues and cells via quantitative real-time polymerase chain reaction (qRT-PCR) analysis, finding that FENDRR was significantly reduced in CC tissues and cells (Fig. 1a, b)

  • Gain-of-function experiments were carried out to confirm the property of FENDRR in CC

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Summary

Introduction

Previous literature has revealed long non-coding RNAs (lncRNAs) are crucial regulators for cell functions and gene expression. LncRNA fetal-lethal non-coding developmental regulatory RNA (FENDRR) was reported as a biological suppressor in several types of human cancers, yet relevant mechanisms and biological effects of FENDRR with regards to cervical cancer (CC) are not explored until now. The 5-year survival rate of patients in advanced CC stage is approximately as low as 15% [4]. Long non-coding RNAs (lncRNAs) are biological regulators in a wide variety of important cellular processes including proliferation, migration and epithelial-mesenchymal transition (EMT) [5, 6]. LncRNA maternally expressed gene 3 (MEG3) inhibits cell proliferation and metastasis in gastric cancer [7]. LncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) drives cell proliferation and EMT in breast cancer [8]

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