Abstract

BackgroundOral squamous cell carcinoma (OSCC) at early stages can be misdiagnosed as an oral ulcer (OU) due to similar symptoms, such as chronic and indurated ulcer. LncRNA NCK1-AS1 has been characterized as a key player in cervical cancer, while its role in OSCC is unknown.MethodsAll participants were selected at Jiangxi Province Tumor Hospital from December 2016 to December 2018. Expression levels of NCK1-AS1 and miR-100 in plasma from both OSCC and OU patients were measured by RT-qPCR. Diagnostic analysis was performed through ROC curve. Potential interactions between NCK1-AS1 and miR-100 were detected by cell transfection experiments. Cell invasion and migration were assessed by Transwell assays.ResultsThe expression of NCK1-AS1 was upregulated in early-stage OSCC patients but not in OU patients. Upregulation of NCK1-AS1 distinguished OSCC patients from OU patients. The expression of miR-100 was inversely correlated with the expression of NCK1-AS1. Overexpression of NCK1-AS1 was followed by promoted OSCC cell invasion and migration. Overexpression of miR-100 did not affect the expression of NCK1-AS1 but inhibited the role of NCK1-AS1.ConclusionsTherefore, NCK1-AS1 may promote the metastasis of OSCC by downregulating miR-100.

Highlights

  • Oral squamous cell carcinoma (OSCC) at early stages can be misdiagnosed as an oral ulcer (OU) due to similar symptoms, such as chronic and indurated ulcer

  • The expression levels of NCK1AS1 in plasma were significantly higher in OSCC group in comparison to that in OU and healthy participant groups (Fig. 1, p < 0.05)

  • No significant differences in the expression levels of plasma NCK1-AS1 were found between OU and control groups (Fig. 1)

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Summary

Introduction

Oral squamous cell carcinoma (OSCC) at early stages can be misdiagnosed as an oral ulcer (OU) due to similar symptoms, such as chronic and indurated ulcer. LncRNA NCK1-AS1 has been characterized as a key player in cervical cancer, while its role in OSCC is unknown. Oral squamous cell carcinoma (OSCC) accounts for more than 80% of head and neck cancer, which is a common malignancy in clinical practices [1, 2]. Alcohol abuse, betel quid chewing consumption and HPV infections have been identified as the major risk factors for OSCC [3]. The molecular mechanism of OSCC pathogenesis remains unclear. OSCC can be diagnosed as other oral lesions [5], leading to delayed treatment. Novel therapeutic targets and accurate diagnostic markers are urgently needed

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