ArticleOncology letters2018
MEG-3-mediated Wnt/β-catenin signaling pathway controls the inhibition of tunicamycin-mediated viability in glioblastoma.
Article in Oncology letters, 2018. 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 It has been retracted, and should not be counted.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 1 paper.
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
1 citing paper in PubMed, 4 citations in OpenAlex.
- LncRNAs associated with glioblastoma: From transcriptional noise to novel regulators with a promising role in therapeutics.Molecular therapy. Nucleic acids · 2021Review
Corrections and comments
- Retraction · 2025-06-30Euphemisms for Plagiarism · Investigation by Journal/Publisher · Investigation by Third Party · Plagiarism of Data · Plagiarism of Image · · See also: https://pubpeer.com/publications/1F6E7718A075DF8253EC4E20AA0A2A
- Retracted
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma is the most common primary brain carcinoma and leads to a poor survival rate of patients worldwide. Results of previous studies have suggested that tunicamycin may inhibit aggressiveness by promoting apoptosis of glioblastoma cells. In the present study, the effects of tunicamycin and its potential molecular mechanisms underlying the viability and aggressiveness of glioblastoma cells were investigated. Western blot analysis, the reverse transcription-quantitative polymerase chain reaction, immunohistochemistry, apoptosis assays and immunofluorescence were employed to examine the effects of tunicamycin on apoptosis, viability, aggressiveness and cell cycle arrest of glioblastoma cells by downregulation of the expression levels of fibronectin and epithelial cadherin.
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.