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Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
miRNA‑1271 inhibits cell proliferation in neuroglioma by targeting fibronectin 1
Jian Gong1, Zhao-Xia Wang2, Zhen-Ying Liu1
1Department of Neurology, Linyi People's Hospital, Linyi, Shandong 276003, P.R. China.
Abstract:
miR-1271 is a multifunctional post-translational modulator, which is involved in several diseases. However, the association between microRNA (miR)‑1271 and fibronectin 1 (FN1) remains to be fully elucidated in neuroglioma. In the present study, it was hypothesized that a post‑translational mechanism of miR‑1271 regulates the expression of FN1 in the progression of neuroglioma. The present study aimed to investigate the clinical significance and underlying molecular mechanisms of miRNA‑1271 in the development of glioma. The miR‑1271 levels in glioma tissues and cell lines were assessed using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). miR‑1271 mimics and inhibitors were transfected to gain or loss of miR‑1271 function. Cell proliferation was analyzed by using an MTT assay. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. The mRNA and protein levels were assessed by RT‑qPCR and western blotting. The results showed that miR‑1271 was downregulated in glioma tumor tissues and cell lines. In addition, it was demonstrated that low levels of miR‑1271 in patients with glioma were correlated with low survival rate. In vitro, the cell viability was significantly suppressed following transfection with miRNA‑1271 mimics and increased following transfection with the miRNA‑1271 inhibitor. The miRNA‑1271 mimics induced cell apoptosis and the miRNA‑1271 inhibitor suppressed cell apoptosis in H4 and U251 cell lines. Furthermore, the 3'‑untranslated region of FN1 was bound by miR‑1271. Therefore, it was concluded that miR‑1271 inhibited glioma cell growth by targeting FN1, and a low level of miR‑1271 in glioma tumor tissues was associated with lower survival rates in patients with glioma.
Insights
MicroRNA-1271 (miR-1271) suppresses neuroglioma growth by targeting fibronectin 1 (FN1). Low miR-1271 levels in glioma patients correlate with reduced survival rates, highlighting its clinical significance.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- MicroRNA (miR)-1271 is implicated in various diseases.
- The specific role of miR-1271 in neuroglioma, particularly its interaction with fibronectin 1 (FN1), requires further investigation.
- Understanding miR-1271's regulatory mechanisms in glioma is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the clinical significance of miR-1271 in glioma development.
- To elucidate the molecular mechanisms by which miR-1271 regulates FN1 expression in neuroglioma.
- To determine the impact of miR-1271 on glioma cell proliferation, apoptosis, and patient survival.
Main Methods:
- Assessed miR-1271 expression in glioma tissues and cell lines using RT-qPCR.
- Utilized miR-1271 mimics and inhibitors for gain and loss-of-function studies in vitro.
- Analyzed cell proliferation (MTT assay), apoptosis, and FN1 expression (RT-qPCR, Western blotting).
- Confirmed direct targeting of FN1 by miR-1271 using bioinformatics and dual-luciferase reporter assays.
Main Results:
- miR-1271 was significantly downregulated in glioma tissues and cell lines.
- Lower miR-1271 levels correlated with reduced patient survival rates.
- miR-1271 overexpression suppressed glioma cell viability and induced apoptosis, while inhibition promoted proliferation and suppressed apoptosis.
- miR-1271 directly targets the 3'-untranslated region of FN1, inhibiting its expression.
Conclusions:
- miR-1271 acts as a tumor suppressor in glioma by targeting FN1.
- Downregulation of miR-1271 contributes to glioma progression and is associated with poor prognosis.
- miR-1271 represents a potential therapeutic target for glioma treatment.
