Evidence map›Paper›PMID 31638257›Full record

ArticleOncology reports2019

miR‑489 promotes apoptosis and inhibits invasiveness of glioma cells by targeting PAK5/RAF1 signaling pathways.

Wei Wang, Luyang Zhang, Wei Gao, Dongyong Zhang, Zilong Zhao, Yijun Bao

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Oncology reports, 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 It has been retracted, and should not be counted.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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 49% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Wei WangDepartment of Neurosurgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Luyang ZhangDepartment of Neurosurgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Wei GaoDepartment of Neurosurgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Dongyong ZhangDepartment of Neurosurgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Zilong ZhaoDepartment of Neurosurgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Yijun BaoDepartment of Neurosurgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
First Hospital of China Medical University · CNChina Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma patients receiving therapy are at a high risk of relapse and rapid progression and, thus, more effective treatments are required. The aim of the present study was to determine the suppressive role of miR‑489 as an alternative therapeutic target for preventing glioma progression. The results of the present study demonstrated that patients with relatively lower levels of expression of miR‑489 had more favorable clinical outcomes. Furthermore, miR‑489 expression was inversely correlated with p21‑activated kinase 5 (PAK5) mRNA expression levels in glioma specimens. A dual luciferase reporter assay revealed that miR‑489 suppressed PAK5 expression by directly targeting the PAK5 3'‑untranslated region. The effects of miR‑489 on cell viability were measured using MTT and Cell Counting Kit‑8 assays. The results demonstrated that ectopic expression of miR‑489 mimic decreased cell viability by interfering with cyclin D1 and c‑Myc signaling. Additionally, the effect of miR‑489 on apoptosis was determined using Hoechst 33258 staining and flow cytometry. The results demonstrated that miR‑489 decreased the activity of RAF1, reduced Bcl‑2 and promoted Bax expression, resulting in increased cell apoptosis. Furthermore, the effect of miR‑489 mimic on cellular motility was assessed using migration and invasion assays. miR‑489 was shown to abolish the PAK5/RAF1/MMP2 pathway, resulting in decreased cell invasion ability. These results indicated that miR‑489 may be involved in PAK5‑mediated regulation of glioma progression, demonstrating the potential therapeutic benefits of targeting miR‑489 in glioma.

Indexed as

ApoptosisGene Expression Regulation, NeoplasticBiomarkers, TumorCell ProliferationGliomaHumansMicroRNAsNeoplasm Invasivenessp21-Activated KinasesPrognosisProto-Oncogene Proteins c-rafSurvival RateTumor Cells, CulturedBiomarkers, TumorMicroRNAsMIRN489 microRNA, humanp21-Activated KinasesPAK5 protein, humanProto-Oncogene Proteins c-rafRaf1 protein, human

Identifiers

PMID31638257
PMCPMC6859450
OpenAlexW2994998536

What OpenQuestion holds

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Registered trials

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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.