STAT3 诱导的长链非编码 RNA ABHD11-AS1 的上调通过调节 miR-1301-3p/STAT3 轴和 PI3K/AKT 信号通路促进甲状腺乳头状癌的肿瘤进展。
STAT3-induced upregulation of lncRNA ABHD11-AS1 promotes tumour progression in papillary thyroid carcinoma by regulating miR-1301-3p/STAT3 axis and PI3K/AKT signalling pathway.
机构信息
Department of Radiation and Oncology, Navy General Hospital, Beijing, China.
Department of Neurosurgery, Navy General Hospital, Beijing, China.
出版信息
Cell Prolif. 2019 Mar;52(2):e12569. doi: 10.1111/cpr.12569. Epub 2019 Jan 18.
OBJECTIVES
Emerging evidences indicated the importance of long non-coding RNAs (lncRNAs) in the tumorigenesis and deterioration of malignant tumours. To our knowledge, the study about lncRNAs in papillary thyroid carcinoma (PTC) is still inadequate. ABHD11-AS1 was highly expressed in the PTC samples of The Cancer Genome Atlas database. This study focused on the biological function and mechanism of lncRNA ABHD11-AS1 in PTC.
MATERIALS AND METHODS
qRT-PCR analysis was used to examine the expression of ABHD11-AS1 in PTC tissues and cell lines. The prognostic significance of ABHD11-AS1 for the patients with PTC was analysed with Kaplan-Meier analysis. The effects of ABHD11-AS1 knockdown on the cell proliferation and metastasis were evaluated by in vitro functional assays and in vivo experiments. The molecular mechanism which contributed to the oncogenic role of ABHD11-AS1 in PTC was explored by conducting mechanism experiments. Rescue assays were carried out for final demonstration.
RESULTS
High expression of ABHD11-AS1 predicted poor prognosis for patients with PTC and promoted cell proliferation and metastasis in vitro and in vivo. ABHD11-AS1 was activated by the transcription factor STAT3. ABHD11-AS1 positively regulated PI3K/AKT signalling pathway. ABHD11-AS1 acted as a competitive endogenous (ce) RNA to upregulate STAT3 by sponging miR-1301-3p.
CONCLUSIONS
STAT3-induced lncRNA ABHD11-AS1 promoted PTC progression by regulating PI3K/AKT signalling pathway and miR-1301-3p/STAT3 axis.
目的
越来越多的证据表明长链非编码 RNA（lncRNA）在肿瘤的发生和恶性肿瘤的恶化中起着重要作用。据我们所知，lncRNA 在甲状腺乳头状癌（PTC）中的研究仍不够充分。ABHD11-AS1 在癌症基因组图谱数据库的 PTC 样本中表达较高。本研究集中于 lncRNA ABHD11-AS1 在 PTC 中的生物学功能和机制。
材料和方法
qRT-PCR 分析用于检测 PTC 组织和细胞系中 ABHD11-AS1 的表达。Kaplan-Meier 分析用于分析 ABHD11-AS1 对 PTC 患者的预后意义。通过体外功能测定和体内实验评估 ABHD11-AS1 敲低对细胞增殖和转移的影响。通过进行机制实验探索有助于 ABHD11-AS1 在 PTC 中致癌作用的分子机制。进行挽救实验以最终证明。
结果
ABHD11-AS1 的高表达预测 PTC 患者预后不良，并在体外和体内促进细胞增殖和转移。ABHD11-AS1 由转录因子 STAT3 激活。ABHD11-AS1 正向调节 PI3K/AKT 信号通路。ABHD11-AS1 通过海绵 miR-1301-3p 作为竞争性内源性（ce）RNA 来上调 STAT3。
结论
STAT3 诱导的 lncRNA ABHD11-AS1 通过调节 PI3K/AKT 信号通路和 miR-1301-3p/STAT3 轴促进 PTC 进展。
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