Evidence map›Paper›PMID 26362401›Full record

ArticleOncotarget2015

Interferon-regulatory factor-1 (IRF1) regulates bevacizumab induced autophagy.

Ji Liang, Yuji Piao, Verlene Henry, Ningyi Tiao, John F de Groot

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 33 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

5 authors at 1 institution in 1 country.

Ji LiangBrain Tumor Center, Department of Neuro-Oncology, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Yuji PiaoBrain Tumor Center, Department of Neuro-Oncology, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Verlene HenryBrain Tumor Center, Department of Neuro-Oncology, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Ningyi TiaoBrain Tumor Center, Department of Neuro-Oncology, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
John F de GrootBrain Tumor Center, Department of Neuro-Oncology, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS CA16672NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

purposeAntiangiogenic therapy is commonly being used for the treatment of glioblastoma. However, the benefits of angiogenesis inhibitors are typically transient and resistance often develops. Determining the mechanism of treatment failure of the VEGF monoclonal antibody bevacizumab for malignant glioma would provide insight into approaches to overcome therapeutic resistance. EXPERIMENTAL

designIn this study, we evaluated the effects of bevacizumab on the autophagy of glioma cells and determined target genes involving in the regulation of bevacizumab-induced autophagy.

resultsWe demonstrated that bevacizumab treatment increased expression of autophagy markers and autophagosome formation in cell culture experiments as well as in in vivo studies. Gene expression profile analysis performed on murine xenograft models of glioblastoma showed increased transcriptional levels of STAT1/IRF1 signaling in bevacizumab resistant tumors compared to control tumors. In vitro experiments showed that bevacizumab treatment increased IRF1 expression in a dose and time dependent manner, which was coincident with bevacizumab-mediated autophagy. Down regulation of IRF1 by shRNA blocked autophagy and increased AIF-dependent apoptosis in bevacizumab-treated glioma cells. Consistently, IRF1 depletion increased the efficacy of anti-VEGF therapy in a glioma xenograft model, which was due to less bevacizumab-promoted autophagy and increased apoptosis in tumors with down-regulated IRF1.

conclusionsThese data suggest that IRF1 may regulate bevacizumab-induced autophagy, and may be one important mediator of glioblastoma resistant to bevacizumab.

Indexed as

Angiogenesis InhibitorsAnimalsApoptosisAutophagyBevacizumabBlotting, WesternBrain NeoplasmsCell ProliferationFluorescent Antibody TechniqueGlioblastomaHumansImmunoenzyme TechniquesInterferon Regulatory Factor-1MiceMice, NudeReal-Time Polymerase Chain ReactionAngiogenesis InhibitorsBevacizumabInterferon Regulatory Factor-1IRF1 protein, humanRNA, MessengerantiangiogenesisautophagybevacizumabIRF1

Identifiers

PMID26362401
PMCPMC4741619
OpenAlexW1815473459

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.