Long Non-coding RNA MINCR Regulates miR-876-5p/GSPT1 Axis to Aggravate Glioma Progression
Autor: | Xiangyun Fan, Xiaoxia Xie, Xing Li, Zheng Li |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Untranslated region Male Mice Nude Biochemistry 03 medical and health sciences Cellular and Molecular Neuroscience Mice 0302 clinical medicine Glioma medicine Gene silencing Animals Humans Gene Cell Proliferation Messenger RNA Chemistry Competing endogenous RNA Brain Neoplasms RNA General Medicine medicine.disease Long non-coding RNA MicroRNAs 030104 developmental biology Cancer research Disease Progression RNA Long Noncoding 030217 neurology & neurosurgery Peptide Termination Factors |
Zdroj: | Neurochemical research. 45(7) |
ISSN: | 1573-6903 |
Popis: | Emerging evidence underlined the crucial roles played by long non-coding RNAs (lncRNAs) in glioma. MINCR has been reported in multiple malignancies. Here, we studied its function and potential mechanism in glioma, which remain unclear. Gene expressions were analyzed by qRT-PCR assay. Both in vitro and in vivo assays were conducted to evaluate the cellular function of MINCR in glioma. The subcellular situation of MINCR was detected by subcellular fractionation and FISH assays. Luciferase reporter, RNA pull-down and RNA immunoprecipitation (RIP) assays were combined to investigate potential mechanisms of relevant genes. MINCR was up-regulated in glioma. MINCR depletion markedly refrained glioma cell proliferation, migration and invasion via sponging miR-876-5p. MiR-876-5p suppressed the malignant behaviors of glioma via binding to GSPT1. MINCR shared the binding sites with the 3'-untranslated region of GSPT1 and prevented the binding of miR-876-5p to GSPT1 mRNA, thus up-regulating the level of GSPT1. Moreover, miR-876 inhibition and GSPT1 up-regulation counteracted the functional effect induced by silencing MINCR on glioma progression. Our findings uncovered that MINCR might aggravated glioma cell proliferation and migration via acting as competing endogenous RNA (ceRNA), indicating prospective novel therapeutic target for glioma. |
Databáze: | OpenAIRE |
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