Evidence map›Paper›PMID 30886199›Full record

ArticleScientific reports2019

Profiling of gallbladder carcinoma reveals distinct miRNA profiles and activation of STAT1 by the tumor suppressive miRNA-145-5p.

Benjamin Goeppert, Felicia Truckenmueller, Alessandro Ori, Valerie Fritz, Thomas Albrecht, Angelika Fraas, Dominique Scherer, Rosa González Silos, Carsten Sticht, Norbert Gretz and 8 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. 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
4.2field-weighted citation impact, top 6% 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, 41 citations in OpenAlex.

  1. Review
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  8. Non-coding RNAs as potential biomarkers of gallbladder cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
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  10. Frontiers in genetics · 2023
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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

18 authors at 4 institutions in 1 country.

Benjamin GoeppertInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Felicia TruckenmuellerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Alessandro OriLeibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.
Valerie FritzInstitute of Biochemistry, Emil-Fischer Zentrum, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Thomas AlbrechtInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Angelika FraasInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Dominique SchererInstitute of Medical Biometry and Informatics, University Hospital Heidelberg, Heidelberg, Germany.
Rosa González SilosInstitute of Medical Biometry and Informatics, University Hospital Heidelberg, Heidelberg, Germany.
Carsten StichtCenter of Medical Research, University Hospital Mannheim, Mannheim, Germany.
Norbert GretzCenter of Medical Research, University Hospital Mannheim, Mannheim, Germany.
Arianeb MehrabiDepartment of General Visceral and Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Germany.
Melanie Bewerunge-HudlerGenomics and Proteomics Core Facility, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0001-9038-7891
Stefan PuschHeidelberg University Hospital, Institute of Pathology, Department of Neuropathology, Heidelberg, Germany and Clinical Cooperation Unit Neuropathology, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0002-3407-4249
Justo Lorenzo BermejoInstitute of Medical Biometry and Informatics, University Hospital Heidelberg, Heidelberg, Germany.
Peter DietrichInstitute of Biochemistry, Emil-Fischer Zentrum, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Peter SchirmacherInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Marcus RennerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Stephanie RoesslerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany. Stephanie.Roessler@med.uni-heidelberg.de.ORCID 0000-0002-5333-5942
Heidelberg University · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEGerman Cancer Research Center · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gallbladder carcinoma (GBC) is a biliary tract cancer with few treatment options and poor prognosis. Radical surgery is the only potentially curative treatment option but most patients diagnosed with GBC are unresectable. Thus, there is a great need for the development of new treatment options including targeted therapy. Here, we aimed at identifying deregulated miRNAs and affected pathways involved in GBC development and progression. We performed global miRNA profiling of 40 GBC and 8 normal gallbladder tissues and identified large differences with 30% of miRNAs being differentially expressed (false discovery rate: FDR < 0.001). We found 24 miRNAs to be differentially regulated in GBC with poor outcome (p < 0.05) of which miR-145-5p was the most downregulated miRNA. Overexpression of miR-145-5p significantly reduced cell proliferation and colony formation. Gene expression analysis of cells expressing miR-145-5p mimics revealed activation of the Signal transducer and activator of transcription 1 (STAT1) signaling pathway which is mainly tumor suppressive. Furthermore, the activation of STAT1 by miR-145-5p was specifically observed in gallbladder carcinoma and cholangiocarcinoma but not in hepatocellular carcinoma cells. The Protein Tyrosine Phosphatase Receptor Type F (PTPRF) is downregulated upon miR-145 expression and may be involved in STAT1 regulation. In addition, we found that the STAT1-regulated protein IRF7 is downregulated in GBC compared to normal gallbladder tissue and low IRF7 expression is associated with significantly lower overall survival of GBC patients. Thus, this study identified GBC patient subgroups and provides new mechanistic insights in the tumor suppressive function of miR-145-5p leading to activation of STAT1 signaling.

Indexed as

AgedCarcinomaCell Line, TumorFemaleGallbladder NeoplasmsGene Expression Regulation, NeoplasticHEK293 CellsHumansInterferon Regulatory Factor-7MaleMicroRNAsReceptor-Like Protein Tyrosine Phosphatases, Class 2STAT1 Transcription FactorInterferon Regulatory Factor-7IRF7 protein, humanMicroRNAsMIRN145 microRNA, humanPTPRF protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 2STAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID30886199
PMCPMC6423323
OpenAlexW2921534199

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.