MicroRNA‑3148 inhibits glioma by decreasing DCUN1D1 and inhibiting the NF‑kB pathway
- Qianghua Xu
- Xiao Chen
- Bin Chen
Affiliations: Department of Neurosurgery, The First People's Hospital of Jingmen, Jingmen, Hubei 448000, P.R. China, Department of Neurosurgery, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei 441021, P.R. China
- Published online on: November 8, 2021 https://doi.org/10.3892/etm.2021.10950
Copyright: © Xu
et al. This is an open access article distributed under the
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Glioma, which originates in the brain, is the most aggressive tumor of the central nervous system. It has been shown that microRNA (miRNA) controls the proliferation, migration and apoptosis of glioma cells. The objective of the present study was to measure microRNA‑3148 (miR‑3148) expression and investigate its impact on the pathogenetic mechanism of glioma. In the present study, reverse transcription‑quantitative real‑time PCR was employed to detect miR‑3148 expression levels in glioma tissues and cell lines. Cell Counting Kit‑8 assay, 5‑ethynyl‑2'‑deoxyuridine assay, and Transwell migration assay were performed to assess the influence of miR‑3148 on the malignant biological behavior of glioma cells. The biological functions of miR‑3148 in glioma were examined via a xenograft tumor growth assay. Furthermore, the association between miR‑3148 and DCUN1D1 was investigated via immunohistochemistry, dual‑luciferase reporter assay and western blotting. It was observed that miR‑3148 was expressed at low levels in glioma cells, and this represented a poor survival rate. In addition, an increased level of miR‑3148 in cells and animal models inhibited glioma cell migration and proliferation. Moreover, miR‑3148 decreased DCUN1D1 and curbed the nuclear factor κ enhancer binding protein (NF‑κB) signaling pathway, thus decreasing the growth of glioma. Thus, miR‑3148 is expressed within glioma tissues at low levels where it suppresses glioma by curbing the NF‑κB pathway and lowering DCUN1D1.