SNHG16 contributes to breast cancer cell migration by competitively binding miR-98 with E2F5
SNHG16 contributes to breast cancer cell migration by competitively binding miR-98 with E2F5
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SNHG16 通过竞争性结合 miR-98 与 E2F5 促进乳腺癌细胞迁移
DOI：
10.1016/j.bbrc.2017.02.094
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发表时间：
2017-04-01
影响因子：
3.1
通讯作者：
Yang, Qifeng
中科院分区：
文献类型：
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作者：
Cai, Chang;Huo, Qiang;Yang, Qifeng
长链非编码RNA（longnoncodingRNA，IncRNA）在肿瘤的发生、发展、增殖和迁移等过程中起着重要作用。在本研究中，我们证明了小核仁RNA宿主基因16（SNHG 16）作为癌基因在乳腺癌细胞迁移。SNHG 16在乳腺癌组织中的表达水平通常高于配对的非癌组织。获得和丧失功能的研究证明，SNHG 16显著促进乳腺癌细胞迁移。我们通过生物信息学分析预测SNHG 16是E2 F转录因子5蛋白（E2 F5）的竞争性内源RNA（ceRNA），并通过相对定量实时PCR（qRT-PCR）、蛋白质印迹、RNA免疫沉淀（RIP）和荧光素酶报告基因分析证实了SNHG 16对E2 F转录因子5蛋白（E2 F5）的调控作用。此外，我们确定了SNHG 16和E2 F5在乳腺癌组织中的正相关性。此外，我们证明了miR-98的强制表达可以部分消除SNHG 16介导的乳腺癌细胞迁移的增加，表明SNHG 16以miR-98依赖的方式促进细胞迁移。总之，我们的研究结果表明，SNHG 16通过竞争性结合miR-98与E2 F5诱导乳腺癌细胞迁移，SNHG 16可以作为乳腺癌治疗的潜在治疗靶点。(C)2017爱思唯尔公司All rights reserved.
Long noncoding RNAs (IncRNAs) have been proved to play important roles in cellular processes of cancer, including the development, proliferation, and migration of cancer cells. In the present study, we demonstrated small nucleolar RNA host gene 16 (SNHG16) as an oncogene on cell migration in breast cancer. Expression levels of SNHG16 were found to be frequently higher in breast cancer tissues than in the paired noncancerous tissues. Gain- and loss-of-function studies proved that SNHG16 significantly promoted breast cancer cell migration. We predicted SNHG16 as a competitive endogenous RNA (ceRNA) of E2F transcription factor 5 protein (E2F5) via competition for the shared miR-98 through bioinformatics analysis, and proved this regulation using relative quantitative real-time PCR (qRT-PCR), western blot, RNA immunoprecipitation (RIP) assay and luciferase reporter assay. In addition, we identified a positive correlation between SNHG16 and E2F5 in breast cancer tissues. Furthermore, we demonstrated that forced expression of miR-98 could partially abrogate SNHG16-mediated increase of breast cancer cells migration, suggesting that SNHG16 promoted cell migration in a miR-98 dependent manner. Taken together, our findings indicated that SNHG16 induces breast cancer cell migration by competitively binding miR-98 with E2F5, and SNHG16 can serve as a potential therapeutic target for breast cancer treatment. (C) 2017 Elsevier Inc. All rights reserved.