Evidence map›Paper›PMID 27329723›Full record

ArticleOncotarget2016

STAT5 induces miR-21 expression in cutaneous T cell lymphoma.

Lise M Lindahl, Simon Fredholm, Claudine Joseph, Boye Schnack Nielsen, Lars Jønson, Andreas Willerslev-Olsen, Maria Gluud, Edda Blümel, David L Petersen, Nina Sibbesen and 16 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  3. Curcumin in treatment of hematological cancers: Promises and challenges.Journal of traditional and complementary medicine · 2024
    Review
  4. miRNA Signature in Early-stage Mycosis Fungoides.Acta dermato-venereologica · 2022
    Article
  5. Article
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  7. Article
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  11. Article
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  14. Review
  15. Article
  16. Review
  17. Oncoimmunology · 2020
    Article
  18. Review
  19. Article
  20. Review
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

26 authors at 10 institutions in 5 countries.

Lise M LindahlDepartment of Dermatology, Aarhus University Hospital, Aarhus, Denmark.
Simon FredholmDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Claudine JosephDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Boye Schnack NielsenBioneer A/S, Hørsholm, Denmark.
Lars JønsonDepartment of Molecular Medicine, Copenhagen University Hospital, Copenhagen, Denmark.
Andreas Willerslev-OlsenDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Maria GluudDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Edda BlümelDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
David L PetersenDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Nina SibbesenDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Tengpeng HuDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Claudia NastasiDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Thorbjørn KrejsgaardDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Ditte JæhgerDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Jenny L PerssonClinical Research Center, Lund University, Malmö, Sweden.
Nigel MonganSchool of Veterinary Medicine and Science, University of Nottingham, Loughborough, United Kingdom.
Mariusz A WasikDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Ivan V LitvinovDivision of Dermatology, Ottawa Hospital Research Institute, University of Ottawa, Ottawa, Ontario, Canada.
Denis SassevilleDivision of Dermatology, McGill University Health Centre, Montréal, Quebec, Canada.
Sergei B KoralovDepartment of Pathology, New York University School of Medicine, New York, NY, USA.
Charlotte M BonefeldDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Carsten GeislerDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Anders WoetmannDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Elisabeth RalfkiaerDepartment of Pathology, Copenhagen University Hospital, Copenhagen, Denmark.
Lars IversenDepartment of Dermatology, Aarhus University Hospital, Aarhus, Denmark.
Niels OdumDepartment of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
University of Copenhagen · DKAarhus University Hospital · DKCopenhagen University Hospital · DKBioneer (Denmark) · DKLund University · SEMcGill University Health Centre · CANew York University · USOttawa Hospital · CAUniversity of Nottingham · GBUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In cutaneous T cell lymphomas (CTCL), miR-21 is aberrantly expressed in skin and peripheral blood and displays anti-apoptotic properties in malignant T cells. It is, however, unclear exactly which cells express miR-21 and what mechanisms regulate miR-21. Here, we demonstrate miR-21 expression in situ in both malignant and reactive lymphocytes as well as stromal cells. qRT-PCR analysis of 47 patients with mycosis fungoides (MF) and Sezary Syndrome (SS) confirmed an increased miR-21 expression that correlated with progressive disease. In cultured malignant T cells miR-21 expression was inhibited by Tofacitinib (CP-690550), a clinical-grade JAK3 inhibitor. Chromatin immunoprecipitation (ChIP) analysis showed direct binding of STAT5 to the miR-21 promoter. Cytokine starvation ex vivo triggered a decrease in miR-21 expression, whereas IL-2 induced an increased miR-21 expression in primary SS T cells and cultured cytokine-dependent SS cells (SeAx). siRNA-mediated depletion of STAT5 inhibited constitutive- and IL-2-induced miR-21 expression in cytokine-independent and dependent T cell lines, respectively. IL-15 and IL-2 were more potent than IL-21 in inducing miR-21 expression in the cytokine-dependent T cells. In conclusion, we provide first evidence that miR-21 is expressed in situ in CTCL skin lesions, induced by IL-2 and IL-15 cytokines, and is regulated by STAT5 in malignant T cells. Thus, our data provide novel evidence for a pathological role of IL-2Rg cytokines in promoting expression of the oncogenic miR-21 in CTCL.

Indexed as

FemaleGene Expression Regulation, NeoplasticHumansLymphoma, T-Cell, CutaneousMaleMicroRNAsSkin NeoplasmsSTAT5 Transcription FactorMicroRNAsMIRN21 microRNA, humanSTAT5 Transcription Factorcutaneous T-cell lymphoma (CTCL)IL-2in situmiR-21STAT5

Identifiers

PMID27329723
PMCPMC5216756
OpenAlexW2441716825

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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.