ArticleMolecular medicine reports2020
Long non‑coding RNA Unigene56159 promotes glioblastoma multiforme cell proliferation and invasion through negatively regulating microRNA‑194‑5p.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Long non-coding RNAs in glioblastoma: from molecular drivers to therapeutic targets.Frontiers in immunology · 2026Review
- A comparison of the expression patterns and diagnostic capability of the ncRNAs NEAT1 and miR-34a in non-obstructive azoospermia and severe oligospermia.Human genomics · 2025Article
- Long Non-Coding RNAs in Malignant Human Brain Tumors: Driving Forces Behind Progression and Therapy.International journal of molecular sciences · 2025Review
- Shedding light on function of long non-coding RNAs (lncRNAs) in glioblastoma.Non-coding RNA research · 2024Review
- circ_0030018 promotes glioma proliferation and metastasis.Translational neuroscience · 2021Article
- Linc01094 Accelerates the Growth and Metastatic-Related Traits of Glioblastoma by Sponging miR-126-5p.OncoTargets and therapy · 2020Article
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Authors and funding
4 authors.
Funding
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Abstract
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.
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