Evidence map›Paper›PMID 26572229›Full record

ArticleRadiation oncology (London, England)2015

The expression level of the transcription factor Aryl hydrocarbon receptor nuclear translocator (ARNT) determines cellular survival after radiation treatment.

Markus Mandl, Maria- Katharina Lieberum, Juergen Dunst, Reinhard Depping

Open access · goldAbstract read
In one paragraph

Article in Radiation oncology (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Von Hippel-Lindau/Hypoxia Inducible Factor Axis in Glioblastoma.International journal of molecular sciences · 2025
    Review
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  9. Role of metabolism in cancer cell radioresistance and radiosensitization methods.Journal of experimental & clinical cancer research : CR · 2018
    Review
  10. Cancer cell international · 2017
    Article
  11. Article
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

4 authors at 1 institution in 1 country.

Markus MandlInstitute of Physiology, Center for Structural and Cell Biology in Medicine, University of Luebeck, Ratzeburger Allee 160, 23562, Luebeck, Germany. markus.mandl@uni-luebeck.de.
Maria- Katharina LieberumInstitute of Physiology, Center for Structural and Cell Biology in Medicine, University of Luebeck, Ratzeburger Allee 160, 23562, Luebeck, Germany. mariakatharina.lieberum@student.uni-luebeck.de.
Juergen DunstKlinik für Strahlentherapie, Universitaetsklinikum Schleswig-Holstein, Campus Luebeck, Ratzeburger Allee 160, 23538, Luebeck, Germany. juergen.dunst@uksh.de.
Reinhard DeppingInstitute of Physiology, Center for Structural and Cell Biology in Medicine, University of Luebeck, Ratzeburger Allee 160, 23562, Luebeck, Germany. reinhard.depping@uni-luebeck.de.
University of Lübeck · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumour hypoxia promotes radioresistance and is associated with poor prognosis. The transcription factor Aryl hydrocarbon receptor nuclear translocator (ARNT), also designated as Hypoxia-inducible factor (HIF)-1β, is part of the HIF pathway which mediates cellular adaptations to oxygen deprivation and facilitates tumour progression. The subunits HIF-1α and ARNT are key players within this pathway. HIF-1α is regulated in an oxygen-dependent manner whereas ARNT is considered to be constitutively expressed. However, there is mounting evidence that certain tumour cells are capable to elevate ARNT in hypoxia which suggests a survival benefit. Therefore the objective of this study was to elucidate effects of an altered ARNT expression level on the cellular response to radiation.

methodsDifferent human cell lines (Hep3B, MCF-7, 786-Owt, 786-Ovhl, RCC4wt and RCC4vhl) originating from various tumour entities (Hepatocellular carcinoma, breast cancer and renal cell carcinoma respectively) were X-irradiated using a conventional linear accelerator. Knockdown of ARNT expression was achieved by transient siRNA transfection. Complementary experiments were performed by forced ARNT overexpression using appropriate plasmids. Presence/absence of ARNT protein was confirmed by Western blot analysis. Clonogenic survival assays were performed in order to determine cellular survival post irradiation. Statistical comparison of two groups was achieved by the unpaired t-test.

resultsThe results of this study indicate that ARNT depletion renders tumour cells susceptible to radiation whereas overexpression of this transcription factor confers radioresistance.

conclusionsThese findings provide evidence to consider ARNT as a drug target and as a predictive marker in clinical applications concerning the response to radiation.

Indexed as

Aryl Hydrocarbon Receptor Nuclear TranslocatorBlotting, WesternCell Line, TumorCell SurvivalGene Knockdown TechniquesHumansRadiation ToleranceReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingTransfectionARNT protein, humanAryl Hydrocarbon Receptor Nuclear TranslocatorRNA, Small Interfering

Identifiers

PMID26572229
PMCPMC4647475
OpenAlexW2173786600

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.