ArticleAmerican journal of translational research2019
MicroRNA-181 inhibits the proliferation, drug sensitivity and invasion of human glioma cells by targeting Selenoprotein K (SELK).
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- Article
- Role of Non-coding RNAs in the Response of Glioblastoma to Temozolomide.Molecular neurobiology · 2025Review
- Selenoprotein K at the intersection of cellular pathways.Archives of biochemistry and biophysics · 2025Review
- Retraction Note: Indirubin exerts anticancer effects on human glioma cells by inducing apoptosis and autophagy.AMB Express · 2024Article
- microRNAs (miRNAs) in Glioblastoma Multiforme (GBM)-Recent Literature Review.International journal of molecular sciences · 2023Review
- NcRNAs: Multi‑angle participation in the regulation of glioma chemotherapy resistance (Review).International journal of oncology · 2022Review
- The Expression Profile of miRNA in Glioma and the Role of miR-339-5p in Glioma.BioMed research international · 2022Article
- Circulating miRNAs as Diagnostic and Prognostic Biomarkers in High-Grade Gliomas.Frontiers in oncology · 2022Article
- Inhibiting of circ-TLK1 inhibits the progression of glioma through down-regulating PANX1 via targeting miR-17-5p.Journal of molecular histology · 2021Article
- Article
- MiR-424-5p Inhibits Proliferation, Invasion and Promotes Apoptosis and Predicts Good Prognosis in Glioma by Directly Targeting BFAR.Pathology oncology research : POR · 2020Article
- Integrated Analysis to Study the Relationship between Tumor-Associated Selenoproteins: Focus on Prostate Cancer.International journal of molecular sciences · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gliomas are aggressive type of brain tumors and cause significant human mortality world over. The frequent relapses, development of drug resistance, the adverse effects of the chemotherapy and dearth of the therapeutic targets form the major hurdles in glioma treatment. Several studies suggest that microRNAs (miRs) are involved in the development and progression of different cancers. Herein, the therapeutic potential of miR-181 was explored in human glioma cells. The results showed that miR-181 is significantly downregulated in human glioma cells. Overexpression of miR-181 caused significant inhibition in the proliferation of U87 and U118 glioma cells. The miR-181 triggered growth inhibition was found to be mainly due to the induction of apoptosis which was concomitant with increase in the Bax/Bcl-2 ratio. Additionally, miR-181 enhanced the chemosensitivity of the glioma cells to temozolomide and suppressed their invasion. Bioinformatic analysis showed that miR-181 exerts its effects by inhibiting the expression of Selenoprotein K (SELK). The expression of SELK was found to be significantly upregulated in glioma cells and silencing of SELK suppressed the proliferation of glioma cells. Nonetheless, overexpression of SELK could nullify the effects of miR-181 on the proliferation of the glioma cells. Taken together, miR-181 may exhibit therapeutic implications in the treatment of glioma.
Indexed as
Identifiers
31737213PMC6834513What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.