Long non-coding RNA TPT1-AS1 promotes cell growth and metastasis in cervical cancer via acting AS a sponge for miR-324-5p.
Long non-coding RNA TPT1-AS1 promotes cell growth and metastasis in cervical cancer via acting AS a sponge for miR-324-5p.
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长非编码RNA TPT1-AS1通过充当miR-324-5p的海绵促进宫颈癌细胞生长和转移
DOI：
10.1186/s13046-018-0846-8
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发表时间：
2018-07-25
期刊：
影响因子：
--
通讯作者：
Jiang X
中科院分区：
文献类型：
--
作者：
Jiang H;Huang G;Zhao N;Zhang T;Jiang M;He Y;Zhou X;Jiang X
背景越来越多的研究证实lncRNA的异常表达在宫颈癌的发生发展中起着重要作用。LncRNA TPT 1-AS 1是一种新的lncRNA，其在CC中的作用及其机制尚不清楚。采用皮下移植瘤模型和尾静脉注射肺转移瘤模型观察肿瘤的生长和转移情况。结果首次证实TPT 1-AS 1在CC组织和细胞系中表达上调。高TPT 1-AS 1与不良预后特征和低生存率显著相关。TPT 1-AS 1过表达和敲低实验表明，TPT 1-AS 1在体外和体内均能促进CC细胞集落形成、增殖、迁移、侵袭和EMT进程。其潜在机制表明TPT 1-AS 1在CC细胞中充当miR-324- 5 p的内源性海绵。获得和丧失实验证实miR-324- 5 p抑制CC细胞的细胞集落形成、增殖、迁移、侵袭和EMT进展，并介导TPT 1-AS 1的生物学效应。进一步的研究证实SP1是miR-324- 5 p的直接靶点，并介导TPT 1-AS 1和miR-324- 5 p在CC中的作用。结论我们首次证明TPT 1-AS 1是CC进展中的致癌lncRNA，也是CC治愈的潜在靶点。
BackgroundIncreasing studies confirmed that abnormal lncRNAs expression play a critical role in cervical cancer (CC) development and progression. LncRNA TPT1-AS1, a novel lncRNA, its role and underlying mechanisms involved in CC remain largely unknown.MethodsColony formation, EdU and Transwell assays were used to determine colony formation, proliferation, migration and invasion in vitro. The subcutaneous tumor model and tail vein injection lung metastasis model were performed to check tumor growth and metastasis in vivo. Luciferase activity and RIP experiment were carried out to determine the interaction between miR-324-5p and TPT1-AS1.ResultsWe demonstrated for the first time that TPT1-AS1 expression was up-regulated in CC tissues and cell lines. High TPT1-AS1 was significantly correlated with adverse prognostic characteristics and poor survival. TPT1-AS1 overexpression and knockdown experiments revealed that TPT1-AS1 promoted cell colony formation, proliferation, migration, invasion and EMT progression of CC cells in vitro and in vivo. The underlying mechanism indicated that TPT1-AS1 functioned as an endogenous sponge for miR-324-5p in CC cells. Gain- and loss- experiment confirmed that miR-324-5p inhibited cell colony formation, proliferation, migration, invasion and EMT progression of CC cells, and mediated the biological effects of TPT1-AS1. Further investigations confirmed that SP1 was a direct target of miR-324-5p and mediated the effects of TPT1-AS1 and miR-324-5p in CC.ConclusionsWe demonstrated for the first time that TPT1-AS1 as an oncogenic lncRNA in CC progression and as a potential target for CC cure.
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