Suppression of miR‑106a‑5p expression inhibits tumorigenesis via increasing CELF‑2 expression in spinal cord glioma
Affiliations: Department of Neurosurgery, The First Affiliated Hospital of University of Science and Technology of China, Hefei, Anhui 230000, P.R. China
- Published online on: June 30, 2021 https://doi.org/10.3892/ol.2021.12888
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Spinal cord glioma is a tumor characterized by high recurrence and mortality rates, and its treatment remains a major challenge. It has been reported that abnormal expression of microRNAs (miRNAs/miRs) is associated with tumor progression. Therefore, the current study aimed to identify novel miRNAs associated with spinal cord glioma. Herein, the expression levels of several miRNAs were determined in human spinal cord glioma and adjacent non‑cancerous tissues by reverse transcription‑quantitative (RT‑qPCR). The results revealed that miR‑106a‑5p expression was markedly upregulated in spinal cord glioma tissues compared with in non‑cancerous tissues. Furthermore, the biological effects of miR‑106a‑5p on spinal cord glioma cells were evaluated by MTT, Transwell and flow cytometric assays. In 0231SCG cells transfected with miR‑106a‑5p inhibitor, cell proliferation, migration and invasion were attenuated, whereas apoptosis was enhanced. A search of the TargetScan database revealed that miR‑106a‑5p directly targeted CUGBP Elav‑like family member 2 (CELF‑2). Western blot and RT‑qPCR experiments further confirmed the association between miR‑106a‑5p and CELF‑2 expression in spinal cord glioma tissues. The current results demonstrated that CELF‑2 was a direct target of miR‑106a‑5p, and that the expression levels of CELF‑2 were negatively associated with those of miR‑106a‑5p. In addition, overexpression of CELF‑2 in spinal cord glioma cells reversed the tumor‑promoting effects of miR‑106a‑5p both in vitro and in vivo. Overall, the aforementioned findings indicated that miR‑106a‑5p, which was highly expressed in spinal cord glioma tissues, may affect the proliferation, migration, invasion and apoptosis of spinal cord glioma cells via targeting CELF‑2, thus indicating a potential approach to the future clinical management of spinal cord glioma.