Evidence map›Paper›PMID 25650658›Full record

ArticleOncotarget2015

Overexpression of IFN-induced protein with tetratricopeptide repeats 3 (IFIT3) in pancreatic cancer: cellular "pseudoinflammation" contributing to an aggressive phenotype.

Hanno Niess, Peter Camaj, Ruth Mair, Andrea Renner, Yue Zhao, Carsten Jäckel, Peter J Nelson, Karl-Walter Jauch, Christiane J Bruns

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

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  15. Emerging Functions of Human IFIT Proteins in Cancer.Frontiers in molecular biosciences · 2019
    Review
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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

9 authors at 3 institutions in 1 country.

Hanno NiessDepartment of Surgery, Medical Center of the Ludwig-Maximilians-University, Campus Grosshadern, Munich, Germany.
Peter CamajDepartment of Surgery, Medical Center of the Otto-von-Guericke-University, Magdeburg, Germany.
Ruth MairDepartment of Surgery, Medical Center of the Ludwig-Maximilians-University, Campus Grosshadern, Munich, Germany.
Andrea RennerDepartment of Surgery, Medical Center of the Ludwig-Maximilians-University, Campus Grosshadern, Munich, Germany.
Yue ZhaoDepartment of Surgery, Medical Center of the Ludwig-Maximilians-University, Campus Grosshadern, Munich, Germany.
Carsten JäckelMedizinische Klinik und Poliklinik IV, Campus Innenstadt, Klinikum der Universitaet Muenchen, Arbeitsgruppe Klinische Biochemie, Munich, Germany.
Peter J NelsonMedizinische Klinik und Poliklinik IV, Campus Innenstadt, Klinikum der Universitaet Muenchen, Arbeitsgruppe Klinische Biochemie, Munich, Germany.
Karl-Walter JauchDepartment of Surgery, Medical Center of the Ludwig-Maximilians-University, Campus Grosshadern, Munich, Germany.
Christiane J BrunsDepartment of Surgery, Medical Center of the Otto-von-Guericke-University, Magdeburg, Germany.
Ludwig-Maximilians-Universität München · DELMU Klinikum · DEOtto-von-Guericke University Magdeburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation contributes to important traits that cancer cells acquire during malignant progression. Gene array data recently identified upregulation of interferon-induced protein with tetratricopeptide repeats 3 (IFIT3) in aggressive pancreatic cancer cells. IFIT3 belongs to the group of interferon stimulated genes (ISG), can be induced by several cellular stress stimuli and by its tetratricopeptide repeats interacts with a multitude of cellular proteins. Upregulation of IFIT3 was confirmed in the aggressive pancreatic cancer cell line L3.6pl compared with its less aggressive cell line of origin, COLO357FG. Transgenic induction of IFIT3 expression in COLO357FG resulted in greater mass of orthotopic tumors and higher prevalence of metastases. Several important traits that mediate malignancy were altered by IFIT3: increased VEGF and IL-6 secretion, chemoresistance and decreased starvation-induced apoptosis. IFIT3 showed binding to JNK and STAT1, the latter being an important inducer of IFIT3 expression. Despite still being alterable by "classical" IFN or NFκB signaling, our findings indicate constitutive - possibly auto-regulated - upregulation of IFIT3 in L3.6pl without presence of an adequate inflammatory stimulus. The transcription factor SOX9, which is linked to regulation of hypoxia-related genes, was identified as a key mediator of upregulation of the oncogene IFIT3 and thereby sustaining a "pseudoinflammatory" cellular condition.

Indexed as

AdenocarcinomaAnimalsApoptosisCell Line, TumorCell ProliferationDose-Response Relationship, DrugDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansInflammationInflammation MediatorsIntracellular Signaling Peptides and ProteinsMaleMice, Inbred BALB CMice, NudePancreatic NeoplasmsIFIT3 protein, humanInflammation MediatorsIntracellular Signaling Peptides and ProteinsSOX9 protein, humanSOX9 Transcription Factor

Identifiers

PMID25650658
PMCPMC4413655
OpenAlexW2139907771

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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.