LncRNA NCK1-AS1 in plasma distinguishes oral ulcer from early-stage oral squamous cell carcinoma.

IF 1.9 3区 生物学 Q2 BIOLOGY Journal of Biological Research-Thessaloniki Pub Date : 2020-11-11 eCollection Date: 2020-12-01 DOI:10.1186/s40709-020-00126-1
Fei Le, Yangqian Ou, Ping Luo, Xiaoming Zhong
{"title":"LncRNA NCK1-AS1 in plasma distinguishes oral ulcer from early-stage oral squamous cell carcinoma.","authors":"Fei Le,&nbsp;Yangqian Ou,&nbsp;Ping Luo,&nbsp;Xiaoming Zhong","doi":"10.1186/s40709-020-00126-1","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>All 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.</p><p><strong>Results: </strong>The 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.</p><p><strong>Conclusions: </strong>Therefore, NCK1-AS1 may promote the metastasis of OSCC by downregulating miR-100.</p>","PeriodicalId":50251,"journal":{"name":"Journal of Biological Research-Thessaloniki","volume":null,"pages":null},"PeriodicalIF":1.9000,"publicationDate":"2020-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s40709-020-00126-1","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biological Research-Thessaloniki","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s40709-020-00126-1","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/12/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"BIOLOGY","Score":null,"Total":0}
引用次数: 9

Abstract

Background: 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.

Methods: All 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.

Results: The 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.

Conclusions: Therefore, NCK1-AS1 may promote the metastasis of OSCC by downregulating miR-100.

Abstract Image

Abstract Image

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
血浆中LncRNA NCK1-AS1可区分口腔溃疡与早期口腔鳞状细胞癌。
背景:口腔鳞状细胞癌(OSCC)早期由于症状相似,如慢性溃疡和硬化性溃疡,容易被误诊为口腔溃疡(OU)。LncRNA NCK1-AS1被认为在宫颈癌中起关键作用,而其在OSCC中的作用尚不清楚。方法:所有受试者均于2016年12月至2018年12月在江西省肿瘤医院就诊。RT-qPCR检测OSCC和OU患者血浆中NCK1-AS1和miR-100的表达水平。通过ROC曲线进行诊断分析。通过细胞转染实验检测NCK1-AS1与miR-100之间潜在的相互作用。Transwell法检测细胞侵袭和迁移。结果:NCK1-AS1在早期OSCC患者中表达上调,而在OU患者中表达上调。NCK1-AS1的上调可将OSCC患者与OU患者区分开来。miR-100表达与NCK1-AS1表达呈负相关。过表达NCK1-AS1会促进OSCC细胞的侵袭和迁移。过表达miR-100不影响NCK1-AS1的表达,但抑制NCK1-AS1的作用。结论:NCK1-AS1可能通过下调miR-100促进OSCC转移。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
5.20
自引率
0.00%
发文量
0
审稿时长
>12 weeks
期刊介绍: Journal of Biological Research-Thessaloniki is a peer-reviewed, open access, international journal that publishes articles providing novel insights into the major fields of biology. Topics covered in Journal of Biological Research-Thessaloniki include, but are not limited to: molecular biology, cytology, genetics, evolutionary biology, morphology, development and differentiation, taxonomy, bioinformatics, physiology, marine biology, behaviour, ecology and conservation.
期刊最新文献
Circ_0000620 acts as an oncogenic factor in gastric cancer through regulating MMP2 expression via sponging miR-671-5p. Peroxiredoxin-6 regulates p38-mediated epithelial-mesenchymal transition in HCT116 colon cancer cells. Nesfatin-1 protects H9c2 cardiomyocytes against cobalt chloride-induced hypoxic injury by modulating the MAPK and Notch1 signaling pathways. LncRNA FBXL19-AS1 promotes proliferation and metastasis of cervical cancer through upregulating COL1A1 as a sponge of miR-193a-5p. CircCNIH4 inhibits gastric cancer progression via regulating DKK2 and FRZB expression and Wnt/β-catenin pathway.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1