Evidence map›Paper›PMID 24518302›Full record

ArticleMolecular oncology2014

NFκB and STAT3 synergistically activate the expression of FAT10, a gene counteracting the tumor suppressor p53.

Yongwook Choi, Jong Kyoung Kim, Joo-Yeon Yoo

Open access · bronzeAbstract read
In one paragraph

Article in Molecular oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

40 citing papers in PubMed, 72 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

3 authors at 2 institutions in 2 countries.

Yongwook ChoiDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Jong Kyoung KimEuropean Bioinformatics Institute, Wellcome Trust Genome Sciences Campus, Cambridge, UK.
Joo-Yeon YooDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea. Electronic address: jyoo@postech.ac.kr.
Pohang University of Science and Technology · KREuropean Bioinformatics Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation is one of the main causes of cancer, yet the molecular mechanism underlying this effect is not fully understood. In this study, we identified FAT10 as a potential target gene of STAT3, the expression of which is synergistically induced by NFκB co-stimulation. STAT3 binding stabilizes NFκB on the FAT10 promoter and leads to maximum induction of FAT10 gene expression. Increased FAT10 represses the transcriptional activity of the tumor suppressor p53, a protein that accelerates the protein degradation of FAT10. This FAT10-p53 double-negative regulation is critical in the control of tumorigenesis, as overexpressed FAT10 facilitates the tumor progression in the solid tumor model. In conclusion, transcriptional synergy between STAT3 and NFκB functions to put weight on FAT10 in the mutually inhibitory FAT10-p53 regulatory loop and thus favors tumorigenesis under inflammatory conditions.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBase SequenceCell LineHep G2 CellsHumansInterleukin-6MiceMice, Inbred C57BLNeoplasmsNF-kappa BPromoter Regions, GeneticSTAT1 Transcription FactorSTAT3 Transcription FactorTranscriptional ActivationTumor Suppressor Protein p53Interleukin-6NF-kappa BSTAT1 Transcription FactorSTAT3 Transcription FactorTumor Suppressor Protein p53UBD protein, humanUbiquitinsFAT10Inflammationp53STAT3Tumorigenesis

Identifiers

PMID24518302
PMCPMC5528625
OpenAlexW1964385468

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.