ArticleMolecular neurobiology2017
MiR-154 Functions as a Tumor Suppressor in Glioblastoma by Targeting Wnt5a.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
8 citing papers in PubMed, 13 citations in OpenAlex.
- LncRNA MIR155HG Promotes Temozolomide Resistance by Activating the Wnt/β-Catenin Pathway Via Binding to PTBP1 in Glioma.Cellular and molecular neurobiology · 2021Article
- MiR-154-5p Suppresses Cell Invasion and Migration Through Inhibiting KIF14 in Nasopharyngeal Carcinoma.OncoTargets and therapy · 2020Article
- MircoRNA-1275 promotes proliferation, invasion and migration of glioma cells via SERPINE1.Journal of cellular and molecular medicine · 2018Article
- MicroRNA-154 Inhibits the Growth and Invasion of Gastric Cancer Cells by Targeting DIXDC1/WNT Signaling.Oncology research · 2018Article
- Migration/Invasion of Malignant Gliomas and Implications for Therapeutic Treatment.International journal of molecular sciences · 2018Review
- Glycogenolysis in Acquired Glioma Resistance to Temozolomide: A Role for the [CaFrontiers in pharmacology · 2018Article
- MicroRNA‑518b functions as a tumor suppressor in glioblastoma by targeting PDGFRB.Molecular medicine reports · 2017Article
- Proof-of-concept study: profile of circulating microRNAs in Bovine serum harvested during acute and persistent FMDV infection.Virology journal · 2017Article
Corrections and comments
- Retraction · 2017-07-05Concerns/Issues about Authorship/Affiliation · Compromised Peer Review · Investigation by Journal/Publisher · Plagiarism of/in Article · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, deregulated microRNA (miRNA) expression contributes to the development and progression of human glioblastoma. The aim of the present study was to evaluate the level of miR-154 and Wnt5a in glioblastoma tissues and cells. We further investigated the molecular mechanisms of miR-154 and Wnt5a in glioblastoma cell lines. In the present study, we found that miR-154 expression was downregulated in glioblastoma tissues and U87, U251, and A172 cells (all p < 0.001). By contrast, Wnt5a was upregulated. Furthermore, we found that overexpression of miR-154 suppressed cell migration and invasion of U87 and U251 cells. Mechanically, overexpression of miR-154 inhibited epithelial-to-mesenchymal transition (EMT) of U87 and U251 cells. Importantly, we identified that the 3' untranslated region (3'-UTR) of Wnt5a was a direct target of miR-154. Luciferase reporter assays confirmed that miR-154 binding to the 3'-UTR regions of Wnt5a inhibited the expression of Wnt5a in U87 and U251 cells. At the same time, overexpressed Wnt5a also reversed EMT inhibited by miR-154. In conclusion, this study suggested that high miR-154 expression suppressed glioblastoma cell migration, invasion, and EMT development through targeting Wnt5a, which may be recommended as a therapeutic target for glioblastoma.
Indexed as
Identifiers
What 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.