Evidence map›Paper›PMID 26894431›Full record

ArticlePloS one2016

Lentivirus-Mediated Knockdown of Astrocyte Elevated Gene-1 Inhibits Growth and Induces Apoptosis through MAPK Pathways in Human Retinoblastoma Cells.

Ying Chang, Bin Li, Xiaolin Xu, Ling Shen, Haixia Bai, Fei Gao, Zhibao Zhang, Jost B Jonas

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2016. 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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Retinoblastoma: present scenario and future challenges.Cell communication and signaling : CCS · 2023
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  10. OncoTargets and therapy · 2017
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Ying ChangBeijing Institute of Ophthalmology, Beijing TongRen Eye Center, Beijing TongRen Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China.
Bin LiBeijing Institute of Ophthalmology, Beijing TongRen Eye Center, Beijing TongRen Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China.
Xiaolin XuBeijing Institute of Ophthalmology, Beijing TongRen Eye Center, Beijing TongRen Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China.
Ling ShenBeijing Institute of Ophthalmology, Beijing TongRen Eye Center, Beijing TongRen Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China.
Haixia BaiBeijing Institute of Ophthalmology, Beijing TongRen Eye Center, Beijing TongRen Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China.
Fei GaoBeijing Institute of Ophthalmology, Beijing TongRen Eye Center, Beijing TongRen Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China.
Zhibao ZhangBeijing Institute of Ophthalmology, Beijing TongRen Eye Center, Beijing TongRen Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China.
Jost B JonasDepartment of Ophthalmology, Medical Faculty Mannheim of the Ruprecht-Karls-University Heidelberg, Mannheim, Germany.
Capital Medical University · CNBeijing Tongren Hospital · CNUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo explore expression and function of astrocyte elevated gene-1 (AEG-1) in human retinoblastoma (RB).

methodsThe expression of AEG-1 in histological sections of human RBs and in RB cell lines was examined using immunohistochemical staining and RT-PCR and Western blotting respectively. We knocked down AEG-1 gene levels by AEG-1-siRNA lentivirus transfection of human RB cell lines SO-RB50 and Y79, and using an MTT assay, we assessed the role of AEG-1 on RB cell proliferation. The biological significance of lentivirus transfection induced AEG-1 down-regulation was examined by assessing the apoptosis rate in the transfected RB cells by Annexin V-APC staining and flow cytometry. We additionally measured the expression of Bcl-2, Bax, cleaved-caspase-3 and caspase-3, and the phosphorylation and non-phosphorylation alternation of MAPKs.

resultsAEG-1 expression was detected to be strongly positive in the histological slides of 35 out of 54 (65%) patients with RB. AEG-1 expression increased significantly (P<0.05) with tumor stage. In the RB cell lines SO-RB50, Y79 and WERI-RB1 as compared with retinal pigment epithelium cells, expression of AEG-1 mRNA and AEG-1 protein was significantly higher. In AEG-1-siRNA lentivirus transfected cell cultures as compared with negative control lentivirus transfected cell cultures, levels of AEG-1 mRNA and of AEG-1 protein (P<0.05) and cell growth rates (P<0.01) were significantly lower, and apoptosis rate (P<0.001), Bax/Bcl-2 ratio and cleaved-caspase-3 protein level were significantly increased. The P-ERK/ERK ratio was significantly decreased in the AEG-1-siRNA lentivirus transfected cell lines.

conclusionsExpression of AEG-1 was associated with RB, in histological slides of patients and in cell culture experiments. Lentivirus transfection induced knockdown of AEG-1 had a tumor suppressive effect, potentially by tumor cell apoptosis induction through inhibition of ERK.

Indexed as

MAP Kinase Signaling SystemApoptosisCaspase 3Cell Adhesion MoleculesCell Line, TumorCell ProliferationExtracellular Signal-Regulated MAP KinasesFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene SilencingGenetic VectorsHumansJNK Mitogen-Activated Protein KinasesLentivirusMaleCaspase 3Cell Adhesion MoleculesExtracellular Signal-Regulated MAP KinasesJNK Mitogen-Activated Protein KinasesMembrane ProteinsMTDH protein, humanProto-Oncogene Proteins c-bcl-2RNA-Binding ProteinsRNA, Small Interfering

Identifiers

PMID26894431
PMCPMC4760765
OpenAlexW2277611632

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.