Evidence map›Paper›PMID 21527635›Full record

ArticleThe Journal of biological chemistry2011

Radiation-triggered tumor necrosis factor (TNF) alpha-NFkappaB cross-signaling favors survival advantage in human neuroblastoma cells.

Jamunarani Veeraraghavan, Mohan Natarajan, Sheeja Aravindan, Terence S Herman, Natarajan Aravindan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

46 citing papers in PubMed, 70 citations in OpenAlex.

  1. Trial
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  7. Radiotherapy and immunology.The Journal of experimental medicine · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. The role of TIGAR in nervous system diseases.Frontiers in aging neuroscience · 2022
    Review
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  15. Article
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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 2 institutions in 1 country.

Jamunarani VeeraraghavanDepartment of Radiation Oncology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.
Mohan Natarajan
Sheeja Aravindan
Terence S Herman
Natarajan Aravindan
The University of Texas Health Science Center at San Antonio · USUniversity of Oklahoma Health Sciences Center · US

Funding

ENHANCED APOPTOSIS BY TARGETING PROTEIN REDOX STATUSR01CA112175 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI NATARAJAN, MOHAN · 2006 to 2009
$705k
NCI NIH HHS R01 CA112175
6 · The paper itself

Abstract

Induced radioresistance in the surviving cancer cells after radiotherapy could be associated with clonal selection leading to tumor regrowth at the treatment site. Previously we reported that post-translational modification of IκBα activates NFκB in response to ionizing radiation (IR) and plays a key role in regulating apoptotic signaling. Herein, we investigated the orchestration of NFκB after IR in human neuroblastoma. Both in vitro (SH-SY5Y, SK-N-MC, and IMR-32) and in vivo (xenograft) studies showed that IR persistently induced NFκB DNA binding activity and NFκB-dependent TNFα transactivation and secretion. Approaches including silencing NFκB transcription, blocking post-translational NFκB nuclear import, muting TNF receptor, overexpression, and physiological induction of either NFκB or TNFα precisely demonstrated the initiation and occurrence of NFκB → TNFα → NFκB positive feedback cycle after IR that leads to and sustains NFκB activation. Selective TNF-dependent NFκB regulation was confirmed with futile inhibition of AP-1 and SP-1 in TNF receptor muted cells. Moreover, IR increased both transactivation and translation of Birc1, Birc2, and Birc5 and induced metabolic activity and clonal expansion. This pathway was further defined to show that IR-induced functional p65 transcription (not NFκB1, NFκB2, or c-Rel) is necessary for activation of these survival molecules and associated survival advantage. Together, these results demonstrate for the first time the functional orchestration of NFκB in response to IR and further imply that p65-dependent survival advantage and initiation of clonal expansion may correlate with an unfavorable prognosis of human neuroblastoma.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisCell Line, TumorCell SurvivalHumansMiceMice, NudeNeoplasm TransplantationNeuroblastomaNF-kappa BPrognosisRadiation, IonizingTime FactorsTumor Necrosis Factor-alphaNF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID21527635
PMCPMC3122217
OpenAlexW2033108034

What OpenQuestion holds

Textmetadata
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.