Upregulation of circ‑ASPH contributes to glioma cell proliferation and aggressiveness by targeting the miR‑599/AR/SOCS2‑AS1 signaling pathway
- Yi Qu
- Li Qi
- Liguo Hao
- Jian Zhu
Affiliations: Department of Neurosurgery, The First Hospital of Qiqihar, Qiqihar Medical University, Qiqihar, Heilongjiang 161000, P.R. China, Department of Nursing, Qiqihar Medical University, Qiqihar, Heilongjiang 161000, P.R. China, Department of Medical Technology, Qiqihar Medical University, Qiqihar, Heilongjiang 161000, P.R. China
- Published online on: March 17, 2021 https://doi.org/10.3892/ol.2021.12649
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Glioma (GM) is the most common type of malignant brain tumor with a high recurrence rate. Circular RNAs (circRNAs) play a key role in mediating tumorigenesis. However, the functions and mechanisms of circRNAs in GM are still not fully understood. A circRNA microarray was performed to identify differentially expressed circRNAs in GM and non‑cancerous specimens. Reverse transcription‑quantitative PCR was used to detect circ‑aspartyl/asparaginyl β‑hydroxylase (ASPH) expression in GM tissues and cells. The clinical importance of circ‑ASPH was investigated using Kaplan‑Meier analysis. The functions of circ‑ASPH were investigated in LN229 and U87MG cells. Bioinformatics, RNA immunoprecipitation, RNA pull‑down and luciferase reporter assays were used to explore the mechanisms of circ‑ASPH in GM. circ‑ASPH levels were upregulated in GM specimens and cells. The prognostic role of circ‑ASPH was identified in patients with GM. Loss/gain of function assays demonstrated that circ‑ASPH increased cell proliferation, migration and invasion in GM cells. Mechanistically, circ‑ASPH counteracted microRNA (miR)‑599‑mediated androgen receptor (AR) suppression by acting as a sponge for miR‑599. Rescue assays indicated that circ‑ASPH facilitated cell progression by regulating AR expression. Moreover, AR activated long non‑coding RNA suppressor of cytokine signaling 2‑antisense RNA 1 (SOCS2‑AS1) expression in GM cells. Taken together, circ‑ASPH/miR‑599/AR/SOCS2‑AS1 signaling may be a promising biomarker/therapeutic target for GM.