Evidence map›Paper›PMID 26083618›Full record

ArticleInflammatory bowel diseases2015

miRNA-26b Overexpression in Ulcerative Colitis-associated Carcinogenesis.

Natalya Benderska, Anna-Lena Dittrich, Sabine Knaup, Tilman T Rau, Clemens Neufert, Sven Wach, Fabian B Fahlbusch, Manfred Rauh, Ralph M Wirtz, Abbas Agaimy and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Inflammatory bowel diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

38 citing papers in PubMed, 63 citations in OpenAlex.

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  18. MicroRNA 452 regulates IL20RA-mediated JAK1/STAT3 pathway in inflammatory colitis and colorectal cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 5 institutions in 4 countries.

Natalya Benderska*Department of Experimental Tumor Pathology, Institute of Pathology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany; †Institute of Pathology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany; ‡First Department of Medicine, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany; Departments of §Urology and ‖Pediatrics and Adolescent Medicine, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany; ¶Stratifyer Molecular Pathology GmbH, Cologne, Germany; **Faculty of School of Chemical and Biotechnology, SASTRA University, Thanjavur, India; ††Institute of Pathology, University Regensburg, Regensburg, Germany; and ‡‡Department of Basic Biomedical Sciences, Laboratory of Biology, School of Medicine, University of Athens, Athens, Greece.
Anna-Lena Dittrich
Sabine Knaup
Tilman T Rau
Clemens Neufert
Sven Wach
Fabian B Fahlbusch
Manfred Rauh
Ralph M Wirtz
Abbas Agaimy
Swetha Srinivasan
Vijayalakshmi Mahadevan
Petra Rümmele
Emmanouela Rapti
Maria Gazouli
Arndt Hartmann
Regine Schneider-Stock
Friedrich-Alexander-Universität Erlangen-Nürnberg · DENational and Kapodistrian University of Athens · GRSASTRA University · INUniversity of Regensburg · DEUrology San Antonio · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLongstanding ulcerative colitis (UC) bears a high risk for development of UC-associated colorectal carcinoma (UCC). The inflammatory microenvironment influences microRNA expression, which in turn deregulates target gene expression. microRNA-26b (miR-26b) was shown to be instrumental in normal tissue growth and differentiation. Thus, we aimed to investigate the impact of miR-26b in inflammation-associated colorectal carcinogenesis.

methodsTwo different cohorts of patients were investigated. In the retrospective group, a tissue microarray with 38 samples from 17 UC/UCC patients was used for miR-26b in situ hybridization and quantitative reverse transcription polymerase chain reaction analyses. In the prospective group, we investigated miR-26b expression in 25 fresh-frozen colon biopsies and corresponding serum samples of 6 UC and 15 non-UC patients, respectively. In silico analysis, Ago2-RNA immunoprecipitation, luciferase reporter assay, quantitative reverse transcription polymerase chain reaction examination, and miR-26b mimic overexpression were employed for target validation.

resultsmiR-26b expression was shown to be upregulated with disease progression in tissues and serum of UC and UCC patients. Using miR-26b and Ki-67 expression levels, an UCC was predicted with high accuracy. We identified 4 novel miR-26b targets (DIP1, MDM2, CREBBP, BRCA1). Among them, the downregulation of the E3 ubiquitin ligase DIP1 was closely related to death-associated protein kinase stabilization along the normal mucosa-UC-UCC sequence. In silico functional pathway analysis revealed that the common cellular pathways affected by miR-26b are highly related to cancerogenesis and the development of gastrointestinal diseases.

conclusionsWe suggest that miR-26b could serve as a biomarker for inflammation-associated processes in the gastrointestinal system. Because miR-26b expression is downregulated in sporadic colon cancer, it could discriminate between UCC and the sporadic cancer type.

Indexed as

AdultArgonaute ProteinsBiomarkers, TumorBRCA1 ProteinCarcinogenesisCeliac DiseaseChildColitis, UlcerativeColonColorectal NeoplasmsCREB-Binding ProteinDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansIn Situ HybridizationAGO2 protein, humanArgonaute ProteinsBiomarkers, TumorBRCA1 ProteinCCNDBP1 protein, humanCREB-Binding ProteinCREBBP protein, humanKi-67 AntigenLuciferasesMDM2 protein, humanMicroRNAsMIRN26 microRNA, humanProto-Oncogene Proteins c-mdm2RNATranscription Factors

Identifiers

PMID26083618
PMCPMC4603667
OpenAlexW2186132811

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.