Evidence map›Paper›PMID 34638467›Full record

ArticleCancers2021

Mir-21 Suppression Promotes Mouse Hepatocarcinogenesis.

Marta Correia de Sousa, Nicolas Calo, Cyril Sobolewski, Monika Gjorgjieva, Sophie Clément, Christine Maeder, Dobrochna Dolicka, Margot Fournier, Laurent Vinet, Xavier Montet and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  6. MicroRNA-21 is a potential therapeutic agent targetingMolecular therapy. Nucleic acids · 2025
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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

15 authors at 5 institutions in 1 country.

Marta Correia de SousaDepartment of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, 1211 Geneva, Switzerland.
Nicolas CaloDepartment of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, 1211 Geneva, Switzerland.
Cyril SobolewskiDepartment of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, 1211 Geneva, Switzerland.ORCID 0000-0002-9404-6290
Monika GjorgjievaDepartment of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, 1211 Geneva, Switzerland.ORCID 0000-0001-8553-7525
Sophie ClémentDivision of Clinical Pathology, Geneva University Hospitals, 1206 Geneva, Switzerland.
Christine MaederDepartment of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, 1211 Geneva, Switzerland.
Dobrochna DolickaDepartment of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, 1211 Geneva, Switzerland.
Margot FournierDepartment of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, 1211 Geneva, Switzerland.
Laurent VinetDepartment of Radiology, Faculty of Medicine, University of Geneva, 1206 Geneva, Switzerland.
Xavier MontetDepartment of Radiology, Faculty of Medicine, University of Geneva, 1206 Geneva, Switzerland.ORCID 0000-0003-2442-5866
Jean-François DufourDepartment for Visceral Surgery and Medicine, University Hospital Bern, 3010 Bern, Switzerland.ORCID 0000-0002-8062-1346
Bostjan HumarDepartment of Visceral & Transplantation Surgery, University Hospital Zürich, 8006 Zürich, Switzerland.
Francesco NegroDivision of Clinical Pathology, Geneva University Hospitals, 1206 Geneva, Switzerland.
Christine SempouxService of Clinical Pathology, University Institute of Pathology, Vaud University Hospital Center, 1011 Lausanne, Switzerland.
Michelangelo FotiDepartment of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, 1211 Geneva, Switzerland.ORCID 0000-0001-7199-4135
University of Geneva · CHUniversity Hospital of Geneva · CHUniversity Hospital of Bern · CHUniversity Hospital of Zurich · CHUniversity of Lausanne · CH

Funding

Swiss National Foundation CRSII3-160717Swiss National Science Foundation 310030-172862Swiss National Science Foundation 320030-20030
6 · The paper itself

Abstract

The microRNA 21 (miR-21) is upregulated in almost all known human cancers and is considered a highly potent oncogene and potential therapeutic target for cancer treatment. In the liver, miR-21 was reported to promote hepatic steatosis and inflammation, but whether miR-21 also drives hepatocarcinogenesis remains poorly investigated in vivo. Here we show using both carcinogen (Diethylnitrosamine, DEN) or genetically (PTEN deficiency)-induced mouse models of hepatocellular carcinoma (HCC), total or hepatocyte-specific genetic deletion of this microRNA fosters HCC development-contrasting the expected oncogenic role of miR-21. Gene and protein expression analyses of mouse liver tissues further indicate that total or hepatocyte-specific miR-21 deficiency is associated with an increased expression of oncogenes such as

Indexed as

fibrosisHCCimmune cellsinflammationmicroRNA 21oncogenesPTENtumor suppressors

Identifiers

PMID34638467
PMCPMC8508272
OpenAlexW3202122008

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.