lncRNA SNHG7 promotes cell proliferation in glioma by acting as a competing endogenous RNA and sponging miR‑138‑5p to regulate EZH2 expression
- Yanyao Deng
- Liuyang Cheng
- Zhicheng Lv
- Hongwei Zhu
- Xiangrui Meng
Affiliations: Department of Neurology, The First Hospital of Changsha, Changsha, Hunan 410005, P.R. China, Department of Hepatopancreatobiliary Surgery, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China, Department of Neurosurgery, Chenzhou First People's Hospital, Chenzhou, Hunan 423000, P.R. China
- Published online on: May 29, 2021 https://doi.org/10.3892/ol.2021.12826
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Glioma is the most common type of primary brain cancer in adults. Accumulating studies have reported that long non‑coding RNAs (lncRNAs) serve a significant role in the initiation and development of glioma. lncRNA small nucleolar RNA host gene 7 (SNHG7) has been previously demonstrated to serve a role in numerous glioma biological processes, including cell proliferation, invasion and migration. The present study aimed to investigate the role of SNHG7 in glioma through reverse transcription‑quantitative PCR, western blotting and cell function assays. The results revealed that SNHG7 expression was upregulated in glioma tissues and cell lines, while microRNA (miR)‑138‑5p expression was downregulated. Moreover, the knockdown of SNHG7 expression decreased the proliferation of glioma cells. Mechanistic studies demonstrated that SNHG7 downregulated miR‑138‑5p expression, which subsequently affected the expression levels of its target gene, enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2). In conclusion, the results of the present study suggested that SNHG7 may act as a competing endogenous RNA to sponge miR‑138‑5p and modulate EZH2 expression. Thus, SNHG7 may enhance glioma proliferation via modulating the miR‑138‑5p/EZH2 signaling axis.