ArticleOncology letters2015
The significance of microRNA-184 on JAK2/STAT3 signaling pathway in the formation mechanism of glioblastoma.
Article in Oncology letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The trial behind it
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- CTR9-mediated JAK2/STAT3 pathway promotes the proliferation, migration, and invasion of human glioma cells.Journal of clinical laboratory analysis · 2021Article
- Noncoding RNAs involved in the STAT3 pathway in glioma.Cancer cell international · 2021Review
- Regulatory effects of microRNA‑184 on osteosarcoma via the Wnt/β‑catenin signaling pathway.Molecular medicine reports · 2018Article
- [ARTICLE WITHDRAWN] Long Noncoding RNA MEG3 Inhibits Cell Proliferation and Metastasis in Chronic Myeloid Leukemia via Targeting miR-184.Oncology research · 2018Article
- Expression of microRNA-184 in glioma.Oncology letters · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma is a type of glioma with a relatively higher degree of malignancy that may result in severe intracranial hypertension and focal symptoms. Surgery is the preferred treatment modality. Combination therapy including radiotherapy, chemotherapy, gene therapy, immunotherapy and targeted therapy have also been employed. However, due to the invasiveness and pathogenesis of the disease, such treatments do not yield satisfactory outcomes. The aim of the present study was to examine the expression of microRNA (miR)-184 in Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway in the mechanism of glioblastoma formation, thus providing a new basis for the mechanism of glioblastoma induction. The LN18 cell line was employed in the present study. After undergoing thawing, culturing and passaging processes, the cells were divided into the set control group, miR-184 mimic group (transfer miR-184 simulator) and miR-184 group. The expression of miR-184 was detected using quantitative polymerase chain reaction. An MTT assay was used to detect the proliferation ability of glioma cells, and clone formation ability was also detected. The cell scratch and invasion assays were used to identify the cell invasion ability. Western blotting was performed to detect the expression level of p-JAK2 and p-STAT3 proteins. The results showed that compared to the control group, the expression of miR-184 in the miR-184 mimic group increased. Cell proliferation, as well as clone formation and invasion ability were enhanced. The number of cells penetrating septum, as well as the expression of p-JAK2 and p-STAT3 proteins were increased. Differences were statistically significant (P<0.05). By contrast, compared to the control group, the expression of miR-184 in the miR-184 inhibitory group decreased. Cell proliferation, as well as clone formation and invasion ability were reduced. The number of cells penetrating septum, as well as the expression of p-JAK2 and p-STAT3 proteins were reduced. Differences were statistically significant (P<0.05). In conclusion, the results of the present study have shown that miR-184 may be involved in the formation of glioblastoma and influence the expression of JAK2/STAT3 signaling pathway.
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