Evidence map›Paper›PMID 28152424›Full record

ArticleNeoplasia (New York, N.Y.)2017

EPSIN 3, A Novel p53 Target, Regulates the Apoptotic Pathway and Gastric Carcinogenesis.

Jinichi Mori, Chizu Tanikawa, Naomi Ohnishi, Yuki Funauchi, Osamu Toyoshima, Koji Ueda, Koichi Matsuda

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 37 citations in OpenAlex.

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  10. Decrease inOncotarget · 2018
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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

7 authors at 2 institutions in 1 country.

Jinichi MoriLaboratory of Clinical Genome sequencing, Department of Computational biology and medical Sciences, Graduate school of Frontier Sciences, The University of Tokyo, Tokyo, Japan.
Chizu TanikawaLaboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Naomi OhnishiProject for Realization of Personalized Cancer Medicine, Genome Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
Yuki FunauchiLaboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Osamu ToyoshimaGastroenterology, Toyoshima Endoscopy Clinic, Tokyo, Japan.
Koji UedaProject for Realization of Personalized Cancer Medicine, Genome Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
Koichi MatsudaLaboratory of Clinical Genome sequencing, Department of Computational biology and medical Sciences, Graduate school of Frontier Sciences, The University of Tokyo, Tokyo, Japan; Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. Electronic address: koichima@ims.u-tokyo.ac.jp.
The University of Tokyo · JPJapanese Foundation For Cancer Research · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimp53 activation by cellular stresses induces the transcription of hundreds of its target genes. To elucidate the entire picture of its downstream pathway, we screened a cDNA microarray dataset of adriamycin-treated HCT116 p53

methodsPotential p53 binding sequences in the EPSIN 3 locus were evaluated by reporter and CHIP assays. To investigate the role of EPSIN 3 in the p53 downstream pathway, we assessed DNA damage-induced apoptosis in EPSIN 3-knockdown HCT116 cells or Epsin 3-deficient mice. In addition, we evaluated EPSIN 3 expression levels in various tissues, including gastric adenocarcinoma, human gastric mucosa with or without Helicobacter pylori infection, and mouse acute gastritis tissues induced by indomethacin.

resultsIn response to DNA damage, p53 induced the expression of EPSIN 3 through the p53 binding elements in the EPSIN 3 promoter and the first intron. Knockdown of EPSIN 3 resulted in resistance to DNA damage-induced apoptosis both in vitro and in vivo. EPSIN 3 expression was down-regulated in gastric cancer tissues compared with normal tissues. In addition, Helicobacter pylori infection and indomethacin-induced acute gastritis repressed EPSIN 3 expression in gastric mucosa.

conclusionsEPSIN 3 is a novel p53 target and a key mediator of apoptosis. Chronic or acute mucosal inflammation as well as p53 inactivation induced down-regulation of EPSIN 3 and subsequently caused apoptosis resistance, which is a hallmark of cancer cells.

Indexed as

Signal TransductionAdaptor Proteins, Vesicular TransportApoptosisCell LineCell ProliferationCell Transformation, NeoplasticGastritisGene Expression Regulation, NeoplasticGene Knockout TechniquesHCT116 CellsHumansProtein BindingProteolysisStomach NeoplasmsStress, PhysiologicalTumor Suppressor Protein p53Adaptor Proteins, Vesicular TransportEPN3 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28152424
PMCPMC5288315
OpenAlexW2582442759

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.