Abstract

BackgroundLong noncoding RNA (lncRNA) LINC00152 (CYTOR) has been reported to be upregulated and to serve as a diagnostic biomarker in multiple types of cancers, including laryngeal squamous cell cancer (LSCC). However, the functional role and molecular mechanisms of LINC00152 in LSCC progression need to be further investigated.MethodsLINC00152 levels in LSCC and adjacent normal tissues were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Gene knockdown of LINC00152 was achieved in LSCC cells by use of small interfering RNA (siRNA). Cell proliferation, apoptosis, migration and invasion were examined by a series of methods. The micoRNA (miRNA) interaction with LINC00152 was screened by starBase v2.0 and confirmed by luciferase reporter activity.ResultsLINC00152 levels in LSCC tissues were significantly higher than those in adjacent normal tissue, and patients with lymph node metastasis or an advanced clinical stage displayed higher LINC00152 expression. Moreover, siRNA-mediated LINC00152 knockdown significantly inhibited the proliferation, migration and invasion of LSCC cells and induced apoptosis in those cells. Mechanistically, LINC00152 functioned as a competing endogenous RNA (ceRNA) sponging miR-613. The inhibitory effect of LINC00152 knockdown on malignant behavior was abrogated by inhibiting miR-613.ConclusionLINC00152 exerts an oncogenic effect on the tumorigenesis of LSCC by sponging miR-613 and may serve as a potential target for treating LSCC.

Highlights

  • Laryngeal squamous cell carcinoma (LSCC) is the most common malignancy of the upper respiratory tract and is the second most common cancer among head and neck malignancies [1]

  • LINC00152 functioned as a competing endogenous RNA sponging miR-613

  • LINC00152 exerts an oncogenic effect on the tumorigenesis of laryngeal squamous cell cancer (LSCC) by sponging miR-613 and may serve as a potential target for treating LSCC

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Summary

Introduction

Laryngeal squamous cell carcinoma (LSCC) is the most common malignancy of the upper respiratory tract and is the second most common cancer among head and neck malignancies [1]. It is crucial to explore the molecular mechanisms underlying LSCC carcinogenesis or progression to develop a more effective therapy target for this disease. LncRNAs have been reported to play crucial roles in diverse cellular processes, including proliferation, apoptosis, differentiation and metastasis [5,6]. A number of studies have demonstrated that lncRNA has the potential as a biomarker or therapy target for LSCC [11,12]. There is urgent need to explore the role of lncRNA in LSCC progression. Long noncoding RNA (lncRNA) LINC00152 (CYTOR) has been reported to be upregulated and to serve as a diagnostic biomarker in multiple types of cancers, including laryngeal squamous cell cancer (LSCC). The functional role and molecular mechanisms of LINC00152 in LSCC progression need to be further investigated

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