Xiao Lei, Wang Weiping, Zhao Jingjing, Xu Hongyan, Li Shaozhen, Yang Xiuhua
Department of Stomatology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China.
Department of Stomatology, Yantaishan Hospital, Yantai, Shandong 264000, P.R. China.
Oncol Lett. 2020 Nov;20(5):164. doi: 10.3892/ol.2020.12024. Epub 2020 Aug 26.
Oral squamous cell carcinoma (OSCC) is the most common malignant tumor of the oral cavity. Emerging evidence indicates that long non-coding (lnc)RNAs play a key role in the cellular processes of tumor cells, including glycolysis, growth and movement. Here, the purpose of this study was to explore the biological functions and potential mechanism of lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in OSCC. OSCC tissues and adjacent matched paraneoplastic normal tissues were collected from 20 OSCC patients. The expression of MALAT1 and miR-101 in OSCC tissues and cell lines (HSC3, SCC9, SCC15 and SCC25) were determined by real-time-polymerase chain reaction (qPCR). Caspase-3, xaspase-8 and EZH2 protein levels were determined by western blot analysis. MALAT1-mediated miRNAs were verified by bioinformatics analysis of StarBase and Luciferase reporter assay. Cell Counting Kit-8 (CCK-8) and Transwell assays were used for investigating MALAT1 effect on cell proliferation and invasion in the OSCC cells. qPCR analysis indicated that MALAT1 expression was obviously increased, and miR-101 was decreased in the OSCC tissues and cell lines. Functional studies revealed that overexpression of MALAT1 promoted OSCC cell proliferation and invasion. Further experiments revealed that miR-101 was a target of MALAT1 and that the miR-101 inhibitor abolished the effect of MALAT1 on OSCC cell proliferation and invasion. Enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) acted as a downstream effecter of MALAT1 in the OSCC cells. Collectively, these findings revealed that upregulation of MALAT1 facilitated OSCC proliferation and invasion by targeting the miR-101/EZH2 axis.
口腔鳞状细胞癌（OSCC）是口腔最常见的恶性肿瘤。新出现的证据表明，长链非编码（lnc）RNA在肿瘤细胞的细胞过程中发挥关键作用，包括糖酵解、生长和迁移。在此，本研究的目的是探讨lncRNA转移相关肺腺癌转录本1（MALAT1）在OSCC中的生物学功能及潜在机制。收集了20例OSCC患者的OSCC组织及相邻配对的癌旁正常组织。通过实时聚合酶链反应（qPCR）测定OSCC组织和细胞系（HSC3、SCC9、SCC15和SCC25）中MALAT1和miR-101的表达。通过蛋白质印迹分析测定半胱天冬酶-3、半胱天冬酶-8和EZH2蛋白水平。通过StarBase的生物信息学分析和荧光素酶报告基因检测验证MALAT1介导的miRNA。使用细胞计数试剂盒-8（CCK-8）和Transwell实验研究MALAT1对OSCC细胞增殖和侵袭的影响。qPCR分析表明，OSCC组织和细胞系中MALAT1表达明显增加，而miR-101表达降低。功能研究显示，MALAT1过表达促进OSCC细胞增殖和侵袭。进一步实验表明，miR-101是MALAT1的靶标，且miR-101抑制剂消除了MALAT1对OSCC细胞增殖和侵袭作用。zeste基因增强子2多梳抑制复合物2亚基（EZH2）在OSCC细胞中作为MALAT1的下游效应因子发挥作用。总的来说，这些发现表明，MALAT1的上调通过靶向miR-101/EZH2轴促进了OSCC的增殖和侵袭。
