Zhu Hong, Zeng Yan, Zhou Chen-Chen, Ye Weiping
Department of Obstetrics and Gynecology, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, No.1665, KongJiang Road, YangPu District, Shanghai 200092, China.
Department of Obstetrics and Gynecology, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, No.1665, KongJiang Road, YangPu District, Shanghai 200092, China.
Arch Biochem Biophys. 2018 Jan 1;637:1-8. doi: 10.1016/j.abb.2017.11.003. Epub 2017 Nov 7.
Long non-coding RNAs (lncRNAs) have been confirmed as crucial regulators in tumorgenesis. Small nucleolar RNA host gene 16 (SNHG16) has been recently uncovered to be a potential oncogene in several types of cancers. However, its expression level and potential role in cervical cancer remain uncertain. In our research, we assessed the expression level of SNHG16 in clinical cervical cancer tissues and cells. We made use of functional assays to determine the biological effects of SNHG16 on cell proliferation and migration of cervical cancer. By employing the bioinformatics analysis tools, we revealed that miR-216-5p could interact with SNHG16 and there existed a negative correlation between the expression levels of miR-216-5p and SNHG16 in cervical cancer specimens. Furthermore, RIP assay, RNA pulldown system and dual luciferase reporter assays confirmed that SNHG16 directly targeted miR-216-5p by harboring the binding sites of microRNA in the SNHG16 sequence. Additionally, bioinformatics analysis provided an evidence that ZEB1 was a potential target of miR-216-5p. Collectively, it was suggested that SNHG16 could serve as an oncogene that promoted tumor progression by acting as an endogenous 'sponge' to regulate miR-216A-5p/ZEB1.
长链非编码RNA（lncRNAs）已被确认为肿瘤发生过程中的关键调节因子。小核仁RNA宿主基因16（SNHG16）最近被发现是几种癌症中的潜在癌基因。然而，其在宫颈癌中的表达水平和潜在作用仍不明确。在我们的研究中，我们评估了SNHG16在临床宫颈癌组织和细胞中的表达水平。我们利用功能试验来确定SNHG16对宫颈癌细胞增殖和迁移的生物学效应。通过使用生物信息学分析工具，我们发现miR-216-5p可以与SNHG16相互作用，并且在宫颈癌标本中miR-216-5p和SNHG16的表达水平之间存在负相关。此外，RNA免疫沉淀试验（RIP）、RNA下拉系统和双荧光素酶报告基因试验证实，SNHG16通过在SNHG16序列中含有微小RNA的结合位点而直接靶向miR-216-5p。此外，生物信息学分析提供了证据表明锌指E盒结合蛋白1（ZEB1）是miR-216-5p的潜在靶点。总的来说，提示SNHG16可以作为一种癌基因，通过作为内源性“海绵”来调节miR-216A-5p/ZEB1，从而促进肿瘤进展。
