Evidence map›Paper›PMID 24587255›Full record

ArticlePloS one2014

A compensatory role of NF-κB to p53 in response to 5-FU-based chemotherapy for gastric cancer cell lines.

Fumitaka Endo, Satoshi S Nishizuka, Kohei Kume, Kazushige Ishida, Hirokatsu Katagiri, Kaoru Ishida, Kei Sato, Takeshi Iwaya, Keisuke Koeda, Go Wakabayashi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 32 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

10 authors at 1 institution in 1 country.

Fumitaka EndoMolecular Therapeutics Laboratory, Iwate Medical University School of Medicine, Morioka, Japan ; Department of Surgery, Iwate Medical University School of Medicine, Morioka, Japan.
Satoshi S NishizukaMolecular Therapeutics Laboratory, Iwate Medical University School of Medicine, Morioka, Japan ; Department of Surgery, Iwate Medical University School of Medicine, Morioka, Japan ; MIAST (Medical Innovation by Advanced Science and Technology) project, Iwate Medical University, Morioka, Japan ; Institute for Biomedical Sciences, Iwate Medical University, Yahaba, Japan.
Kohei KumeMolecular Therapeutics Laboratory, Iwate Medical University School of Medicine, Morioka, Japan ; Department of Surgery, Iwate Medical University School of Medicine, Morioka, Japan ; MIAST (Medical Innovation by Advanced Science and Technology) project, Iwate Medical University, Morioka, Japan ; Institute for Biomedical Sciences, Iwate Medical University, Yahaba, Japan.
Kazushige IshidaMolecular Therapeutics Laboratory, Iwate Medical University School of Medicine, Morioka, Japan ; Department of Surgery, Iwate Medical University School of Medicine, Morioka, Japan.
Hirokatsu KatagiriMolecular Therapeutics Laboratory, Iwate Medical University School of Medicine, Morioka, Japan ; Department of Surgery, Iwate Medical University School of Medicine, Morioka, Japan.
Kaoru IshidaMolecular Therapeutics Laboratory, Iwate Medical University School of Medicine, Morioka, Japan ; Department of Surgery, Iwate Medical University School of Medicine, Morioka, Japan.
Kei SatoMolecular Therapeutics Laboratory, Iwate Medical University School of Medicine, Morioka, Japan ; Department of Surgery, Iwate Medical University School of Medicine, Morioka, Japan.
Takeshi IwayaMolecular Therapeutics Laboratory, Iwate Medical University School of Medicine, Morioka, Japan ; Department of Surgery, Iwate Medical University School of Medicine, Morioka, Japan.
Keisuke KoedaDepartment of Surgery, Iwate Medical University School of Medicine, Morioka, Japan.
Go WakabayashiDepartment of Surgery, Iwate Medical University School of Medicine, Morioka, Japan.
Iwate Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite of remarkable improvement of postoperative 5-FU-based adjuvant chemotherapy, the relapse rate of gastric cancer patients who undergo curative resection followed by the adjuvant chemotherapy remains substantial. Therefore, it is important to identify prediction markers for the chemotherapeutic efficacy of 5-FU. We recently identified NF-κB as a candidate relapse prediction biomarker in gastric cancer. To evaluate the biological significance of NF-κB in the context of 5-FU-based chemotherapy, we analyzed the NF-κB-dependent biological response upon 5-FU treatment in gastric cancer cell lines. Seven genes induced by 5-FU treatment in an NF-κB-dependent manner were identified, five of which are known p53 targets. Knockdown of RELA, which encodes the p65 subunit of NF-κB, decreased both p53 and p53 target protein levels. In contrast, NF-κB was not affected by TP53 knockdown. We also demonstrated that cell lines bearing Pro/Pro homozygosity in codon72 of p53 exon4, which is important for NF-κB binding to p53, are more resistant to 5-FU than those with Arg/Arg homozygosity. We conclude that NF-κB plays an important role in the response to 5-FU treatment in gastric cancer cell lines, with a possible compensatory function of p53. These results suggest that NF-κB is a potential 5-FU-chemosensitivity prediction marker that may reflect 5-FU-induced stress-response pathways, including p53.

Indexed as

Antimetabolites, AntineoplasticCell Line, TumorCodonDrug Resistance, NeoplasmFluorouracilGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansNF-kappa BProtein BindingProtein TransportStomach NeoplasmsTranscription Factor RelATumor Suppressor Protein p53Antimetabolites, AntineoplasticCodonFluorouracilNF-kappa BTranscription Factor RelATumor Suppressor Protein p53

Identifiers

PMID24587255
PMCPMC3937424
OpenAlexW1986758873

What OpenQuestion holds

Textmetadata
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.