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长链非编码RNA MCM3AP-AS1通过抑制miR-363-5p促进口腔鳞状细胞癌的发展。

lncRNA MCM3AP-AS1 promotes the development of oral squamous cell carcinoma by inhibiting miR-363-5p.

作者信息

Hou Chao, Wang Xu, Du Bo

机构信息

Department of Stomatology, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277100, P.R. China.

出版信息

Exp Ther Med. 2020 Aug;20(2):978-984. doi: 10.3892/etm.2020.8738. Epub 2020 May 12.

DOI:10.3892/etm.2020.8738
PMID:32742341
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7388416/
Abstract

The aim of the present study was to study the mechanism of the long non-coding (lnc)RNA MCM3AP-AS1 in the development of oral squamous cell carcinoma (OSCC). Patients with OSCC (n=36) volunteered to join the study, and their tumor/normal tissues were collected. MCM3AP-AS1 and microRNA (miR)-363-5p expression in tissues and cells was determined by reverse transcription-quantitative (RT-q)PCR. Following transfection, a CCK-8 assay and Transwell experiments were conducted to explore the effects of MCM3AP-AS1 on OSCC cell proliferation, migration and invasion. The interaction between MCM3AP-AS1 and miR-363-5p was detected by luciferase reporter gene assay. RT-qPCR analysis demonstrated significantly higher MCM3AP-AS1 expression in tumor tissues or OSCC cells compared with normal tissues or human oral keratinocytes cells (P<0.05). A high MCM3AP-AS1 level was associated with poor prognosis in OSCC patients (P<0.05 or P<0.01). Compared to the small interfering (si)-negative control (NC) group, OSCC cells of si-MCM3AP-AS1 group exhibited markedly lower optical density (at 450 nm) value and relative migration and invasion (P<0.05). miR-363-5p was directly inhibited by MCM3AP-AS1. OSCC cells of si-MCM3AP-AS1 + inhibitor-NC group exhibited clearly lower relative proliferation, migration and invasion compared with cells of si-NC + inhibitor-NC group and si-MCM3AP-AS1 + miR-363-5p inhibitor group (P<0.05). MCM3AP-AS1 promoted OSCC cells proliferation, migration and invasion by inhibiting miR-363-5p.

摘要

本研究旨在探究长链非编码(lnc)RNA MCM3AP-AS1在口腔鳞状细胞癌(OSCC)发生发展中的作用机制。36例OSCC患者自愿参与本研究,并收集其肿瘤组织及正常组织。采用逆转录定量(RT-q)PCR法检测组织及细胞中MCM3AP-AS1和微小RNA(miR)-363-5p的表达。转染后,进行CCK-8实验和Transwell实验,以探究MCM3AP-AS1对OSCC细胞增殖、迁移及侵袭能力的影响。采用荧光素酶报告基因实验检测MCM3AP-AS1与miR-363-5p之间的相互作用。RT-qPCR分析显示,与正常组织或人口腔角质形成细胞相比,肿瘤组织或OSCC细胞中MCM3AP-AS1的表达显著升高(P<0.05)。MCM3AP-AS1高表达与OSCC患者预后不良相关(P<0.05或P<0.01)。与小干扰(si)阴性对照组相比,si-MCM3AP-AS1组OSCC细胞的光密度(450nm处)值及相对迁移和侵袭能力显著降低(P<0.05)。MCM3AP-AS1可直接抑制miR-363-5p。与si-NC + inhibitor-NC组和si-MCM3AP-AS1 + miR-363-5p抑制剂组相比,si-MCM3AP-ASl + inhibitor-NC组OSCC细胞的相对增殖、迁移及侵袭能力明显降低(P<0.05)。MCM3AP-AS1通过抑制miR-363-5p促进OSCC细胞的增殖、迁移及侵袭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc3/7388416/863f2de445d1/etm-20-02-0978-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc3/7388416/fdb3157527cc/etm-20-02-0978-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc3/7388416/746f938850c4/etm-20-02-0978-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc3/7388416/c023b70c404c/etm-20-02-0978-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc3/7388416/863f2de445d1/etm-20-02-0978-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc3/7388416/fdb3157527cc/etm-20-02-0978-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc3/7388416/746f938850c4/etm-20-02-0978-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc3/7388416/c023b70c404c/etm-20-02-0978-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc3/7388416/863f2de445d1/etm-20-02-0978-g03.jpg

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