Long non‑coding RNA Unigene56159 promotes glioblastoma multiforme cell proliferation and invasion through
negatively regulating microRNA‑194‑5p
- Guangyu Jiang
- Hang Dong
- Yu Dong
- Xinyu Yang
Affiliations: Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China, Department of Hematology, Shenzhen Seventh People's Hospital/Shenzhen Yantian District People's Hospital (Group), Shenzhen, Guangdong 518109, P.R. China, Department of Neurosurgery, Shenzhen SAMII Medical Center, Shenzhen, Guangdong 518118, P.R. China
- Published online on: November 26, 2019 https://doi.org/10.3892/mmr.2019.10852
Copyright : © Jiang
et al. This is an open access article distributed under the
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Commons Attribution License [CC BY 4.0].
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Long non‑coding RNAs (lncRNA) serve a vital role in tumor progression. The present study identified a fundamental role for a novel lincRNA, Unigene56159, in the progression of glioblastoma (GBM). Unigene56159 gene expression was found to be significantly upregulated in tissue samples from patients with GBM as well as in GBM cell lines by reverse transcription‑quantitative PCR, while microRNA (miR)‑194‑5p expression levels were decreased. This higher expression level of Unigene56159 was positively correlated with poor overall survival in patients with GBM. However, the mechanism by which this occurs remains to be elucidated. lncRNAs may act as endogenous miRNA sponges for binding to miRNAs or participating in the competitive endogenous RNAs (ceRNA) regulatory network. Small interfering RNA (siRNA) was used to silence the expression of Unigene56159 and inhibit the proliferation and invasion of GBM cell lines by MTT and Transwell assay. Unigene56159 was found to directly interact with miR‑194‑5p, and rescue assay was performed to further confirm that Unigene56159 contributed to glioma progression by regulating miR‑194‑5p. Thus, Unigene56159 may function as a competing endogenous RNA by sequestering miR‑194‑5p in GBM cells. These findings suggested that Unigene56159 may serve an oncogenic role in GBM and may promote disease progression through interacting with miR‑194‑5p. This could be a potential therapeutic target for the treatment of GBM.