Abstract

BackgroundLong noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) plays key role in the progression of some human cancers. However, the role of NEAT1 in human laryngeal squamous cell cancer (LSCC) is still unknown. We therefore investigated the expression and function of NEAT1 in LSCC.MethodsNEAT1 level in LSCC and adjacent non-neoplastic tissues were detected by qRT-PCR. NEAT1 was knockdown in LSCC cells and cell proliferation, apoptosis and cell cycle were examined. The growth of xenografts with NEAT1 knockdown LSCC cells was analyzed.ResultsNEAT1 level was significantly higher in LSCC than in corresponding adjacent non-neoplastic tissues, and patients with neck nodal metastasis or advanced clinical stage had higher NEAT1 expression. Moreover, siRNA mediated NEAT1 knockdown significantly inhibited the proliferation and induced apoptosis and cell cycle arrest at G1 phase in LSCC cells. The growth of LSCC xenografts was significantly suppressed by the injection of NEAT1 siRNA lentivirus. Furthermore, NEAT1 regulated CDK6 expression in LSCC cells which was mediated by miR-107.ConclusionNEAT1 plays an oncogenic role in the tumorigenesis of LSCC and may serve as a potential target for therapeutic intervention.

Highlights

  • Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) plays key role in the progression of some human cancers

  • NEAT1 is overexpressed in laryngeal squamous cell cancer (LSCC) qPCR analysis showed that NEAT1 levels were significantly higher in LSCC tumor tissues than in adjacent nonneoplastic tissues (3.041 ± 0.709 fold, P < 0.01)

  • We found that NEAT1 knockdown inhibited Hep-2 cell migration (Fig. 3)

Read more

Summary

Introduction

Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) plays key role in the progression of some human cancers. The role of NEAT1 in human laryngeal squamous cell cancer (LSCC) is still unknown. We investigated the expression and function of NEAT1 in LSCC. Laryngeal squamous cell carcinoma (LSCC) is one of the most common malignancies in the head and neck [1]. We and others have focused on the role of aberrant expression of noncoding RNAs in LSCC [2,3,4,5,6]. We demonstrated that NEAT1 upregulated cyclin-dependent kinase 6 (CDK6) through inhibiting the expression of miR-107. These results provide the evidence that NEAT1-miR-107-CDK6 regulatory network promotes LSCC

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call