Evidence map›Paper›PMID 25695505›Full record

ArticlePloS one2015

NF-κB regulates caspase-4 expression and sensitizes neuroblastoma cells to Fas-induced apoptosis.

Hai-Jie Yang, Mian Wang, Lei Wang, Bin-Feng Cheng, Xiao-Yu Lin, Zhi-Wei Feng

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

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  11. Transcriptional Regulation of Inflammasomes.International journal of molecular sciences · 2020
    Review
  12. Upregulation ofInternational journal of molecular sciences · 2020
    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

6 authors at 1 institution in 1 country.

Hai-Jie YangCollege of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Mian WangCollege of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Lei WangCollege of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Bin-Feng ChengCollege of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Xiao-Yu LinCollege of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Zhi-Wei FengCollege of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Xinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Found in neurons and neuroblastoma cells, Fas-induced apoptosis and accompanied activation of NF-κB signaling were thought to be associated with neurodegenerative diseases. However, the detailed functions of NF-κB activation in Fas killing and the effect of NF-κB activation on its downstream events remain unclear. Here, we demonstrated that agonistic Fas antibody induces cell death in a dose-dependent way and NF-κB signaling is activated as well, in neuroblastoma cells SH-EP1. Unexpectedly, NF-κB activation was shown to be pro-apoptotic, as suggested by the reduction of Fas-induced cell death with either a dominant negative form of IκBα (DN-IκBα) or an IκB kinase-specific inhibitor. To our interest, when analyzing downstream events of NF-κB signaling, we found that DN-IκBα only suppressed the expression of caspase-4, but not other caspases. Vice versa, enhancement of NF-κB activity by p65 (RelA) overexpression increased the expression of caspase-4 at both mRNA and protein levels. More directly, results from dual luciferase reporter assay demonstrated the regulation of caspase-4 promoter activity by NF-κB. When caspase-4 activity was blocked by its dominant negative (DN) form, Fas-induced cell death was substantially reduced. Consistently, the cleavage of PARP and caspase-3 induced by Fas was also reduced. In contrast, the cleavage of caspase-8 remained unaffected in caspase-4 DN cells, although caspase-8 inhibitor could rescue Fas-induced cell death. Collectively, these data suggest that caspase-4 activity is required for Fas-induced cell apoptosis and caspase-4 may act upstream of PARP and caspase-3 and downstream of caspase-8. Overall, we demonstrate that NF-κB can mediate Fas-induced apoptosis through caspase-4 protease, indicating that caspase-4 is a new mediator of NF-κB pro-apoptotic pathway in neuroblastoma cells.

Indexed as

ApoptosisGene Expression Regulation, NeoplasticCaspase 3Caspase 8Caspases, InitiatorCell Line, TumorDown-Regulationfas ReceptorHumansI-kappa B ProteinsNeuroblastomaNF-kappa BNF-KappaB Inhibitor alphaSignal TransductionUp-RegulationCASP4 protein, humanCaspase 3Caspase 8Caspases, Initiatorfas ReceptorI-kappa B ProteinsNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, human

Identifiers

PMID25695505
PMCPMC4335045
OpenAlexW1992920643

What OpenQuestion holds

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LicenceCC BY
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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.