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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.

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机构: [1]Department of Radiation and Oncology, Navy General Hospital, Beijing, China [2]Department of Neurosurgery, Navy General Hospital, Beijing, China [3]TCM‐Integrated Cancer Center of Southern Medical University, GuangZhou, Guangdong, China [4]AnHui Medical University, HeFei, Anhui, China
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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. 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. 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. STAT3-induced lncRNA ABHD11-AS1 promoted PTC progression by regulating PI3K/AKT signalling pathway and miR-1301-3p/STAT3 axis. © 2019 The Authors. Cell Proliferation Published by John Wiley & Sons Ltd.

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出版当年[2018]版:
大类 | 2 区 生物
小类 | 3 区 细胞生物学
最新[2025]版:
大类 | 1 区 生物学
小类 | 1 区 细胞生物学
第一作者:
第一作者机构: [1]Department of Radiation and Oncology, Navy General Hospital, Beijing, China [*1]Department of Radiation and Oncology, Navy General Hospital, Beijing, China.
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通讯机构: [1]Department of Radiation and Oncology, Navy General Hospital, Beijing, China [*1]Department of Radiation and Oncology, Navy General Hospital, Beijing, China.
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