ArticleRSC advances2019
Retracted Article: Long noncoding RNA PTPRG-AS1 regulates growth of glioma cells by sponging miR-185-5p.
Article in RSC advances, 2019. 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 It has been retracted, and should not be counted.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 2 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
2 citing papers in PubMed.
- Upregulation of long-noncoding RNA PTPRG-AS1 can predict the poor prognosis and promote migration and invasion in patients with osteosarcoma.Oncology letters · 2021Article
- Long non-coding RNAs as the critical factors during tumor progressions among Iranian population: an overview.Cell & bioscience · 2020Review
Corrections and comments
- Retracted
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have found that long noncoding RNA (lncRNA) protein tyrosine phosphatase, receptor type, G, antisense (PTPRG-AS1) was upregulated in glioma cells. Our study aimed to explore the detailed molecular mechanisms of PTPRG-AS1 involved in glioma progression. qRT-PCR assay was performed to measure the expressions of PTPRG-AS1 and microRNA-185-5p (miR-185-5p). Cell viability, migration, invasion, and apoptosis were determined by CCK-8 assay, colony formation assay, transwell assay, and flow cytometry assay. Autophagy was evaluated using GFP-LC3 puncta analysis and western blot. Luciferase reporter and RIP assays were employed to explore the association between PTPRG-AS1 and miR-185-5p. Our data showed PTPRG-AS1 was upregulated in glioma cells and tissues. Besides, high expression of PTPRG-AS1 was positively associated with a low survival rate. Upregulation of PTPRG-AS1 promoted proliferation, migration, invasion, colony formations, and autophagy, and inhibited cell apoptosis in U373-MG cells. By contrast, PTPRG-AS1 downregulation had the inverse effect in SHG44 cells. PTPRG-AS1 negatively regulated the expression of miR-185-5p in U373-MG and SHG44 cells and the expression of miR-185-5p was decreased in glioma tissues and cells. In addition, miR-185-5p overexpression suppressed proliferation, metastasis, colony formations, and autophagy, while inducing cell apoptosis in SHG44 cells. As expected, miR-185-5p depletion exhibited the inverse effect in U373-MG cells. Enhanced expression of miR-185-5p attenuated the effect of PTPRG-AS1 upregulation on U373-MG cells, while silencing of miR-185-5p undermined the effect of downregulation of PTPRG-AS1 on SHG44 cells. Our data disclosed that LncRNA PTPRG-AS1 was upregulated in glioma cells and tissues. PTPRG-AS1 regulated glioma proliferation, invasion, migration, apoptosis and autophagy by sponging miR-185-5p
Identifiers
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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.