Evidence map›Paper›PMID 29416731›Full record

ArticleOncotarget2018

Comparative proteomics as a tool for identifying specific alterations within interferon response pathways in human glioblastoma multiforme cells.

Irina A Tarasova, Alesya V Tereshkova, Anna A Lobas, Elizaveta M Solovyeva, Alena S Sidorenko, Vladimir Gorshkov, Frank Kjeldsen, Julia A Bubis, Mark V Ivanov, Irina Y Ilina and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 8 institutions in 2 countries.

Irina A Tarasova *Talrose Institute for Energy Problems of Chemical Physics, Russian Academy of Sciences, 119334 Moscow, Russia.
Alesya V Tereshkova *Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia.
Anna A LobasTalrose Institute for Energy Problems of Chemical Physics, Russian Academy of Sciences, 119334 Moscow, Russia.
Elizaveta M SolovyevaTalrose Institute for Energy Problems of Chemical Physics, Russian Academy of Sciences, 119334 Moscow, Russia.
Alena S SidorenkoEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia.
Vladimir GorshkovDepartment of Biochemistry and Molecular Biology, University of Southern Denmark, 5230 Odense M, Denmark.
Frank KjeldsenDepartment of Biochemistry and Molecular Biology, University of Southern Denmark, 5230 Odense M, Denmark.
Julia A BubisTalrose Institute for Energy Problems of Chemical Physics, Russian Academy of Sciences, 119334 Moscow, Russia.
Mark V IvanovTalrose Institute for Energy Problems of Chemical Physics, Russian Academy of Sciences, 119334 Moscow, Russia.
Irina Y IlinaOrekhovich Institute of Biomedical Chemistry, 119121 Moscow, Russia.
Sergei A MoshkovskiiOrekhovich Institute of Biomedical Chemistry, 119121 Moscow, Russia.
Peter M ChumakovEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia.
Mikhail V GorshkovTalrose Institute for Energy Problems of Chemical Physics, Russian Academy of Sciences, 119334 Moscow, Russia.
Institute of Energy Problems of Chemical Physics · RUMoscow Institute of Physics and Technology · RUUniversity of Southern Denmark · DKChumakov Institute of Poliomyelitis and Viral Encephalitides · RUEngelhardt Institute of Molecular Biology · RUInstitute of Biomedical Chemistry · RUPirogov Russian National Research Medical University · RURussian Academy of Sciences · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An acquisition of increased sensitivity of cancer cells to viruses is a common outcome of malignant progression that justifies the development of oncolytic viruses as anticancer therapeutics. Studying molecular changes that underlie the sensitivity to viruses would help to identify cases where oncolytic virus therapy would be most effective. We quantified changes in protein abundances in two glioblastoma multiforme (GBM) cell lines that differ in the ability to induce resistance to vesicular stomatitis virus (VSV) infection in response to type I interferon (IFN) treatment. In IFN-treated samples we observed an up-regulation of protein products of some IFN-regulated genes (IRGs). In total, the proteome analysis revealed up to 20% more proteins encoded by IRGs in the glioblastoma cell line, which develops resistance to VSV infection after pre-treatment with IFN. In both cell lines protein-protein interaction and signaling pathway analyses have revealed a significant stimulation of processes related to type I IFN signaling and defense responses to viruses. However, we observed a deficiency in STAT2 protein in the VSV-sensitive cell line that suggests a de-regulation of the JAK/STAT/IRF9 signaling. The study has shown that the up-regulation of IRG proteins induced by the IFNα treatment of GBM cells can be detected at the proteome level. Similar analyses could be applied for revealing functional alterations within the antiviral mechanisms in glioblastoma samples, accompanying by acquisition of sensitivity to oncolytic viruses. The approach can be useful for discovering the biomarkers that predict a potential sensitivity of individual glioblastoma tumors to oncolytic virus therapy.

Indexed as

comparative proteomicsglioblastoma multiformeinterferon signaling alterationsJAK/STAT pathwayoncolytic virotherapy

Identifiers

PMID29416731
PMCPMC5788599
OpenAlexW2768527507

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.