Evidence map›Paper›PMID 20388916›Full record

ArticleScience signaling2010

Identification of the miR-106b~25 microRNA cluster as a proto-oncogenic PTEN-targeting intron that cooperates with its host gene MCM7 in transformation.

Laura Poliseno, Leonardo Salmena, Luisa Riccardi, Alessandro Fornari, Min Sup Song, Robin M Hobbs, Paolo Sportoletti, Shorheh Varmeh, Ainara Egia, Giuseppe Fedele and 3 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Science signaling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 252 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
252citing papers in PubMed, 1 pooled it
19.6field-weighted citation impact, top 1% 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

252 citing papers in PubMed, 1 synthesis or guideline pooled it, 409 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. The cross-talk between GSK-3β, RKIP, and PTEN as potential targets for therapeutic implications in cancer: a comprehensive insight.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2026
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  19. Cancer resistance via the downregulation of the tumor suppressorsExploration of targeted anti-tumor therapy · 2023
    Review
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192 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

13 authors at 5 institutions in 1 country.

Laura PolisenoCancer Genetics Program, Beth Israel Deaconess Cancer Center, Harvard Medical School, Boston, MA 02215, USA.
Leonardo Salmena
Luisa Riccardi
Alessandro Fornari
Min Sup Song
Robin M Hobbs
Paolo Sportoletti
Shorheh Varmeh
Ainara Egia
Giuseppe Fedele
Lucia Rameh
Massimo Loda
Pier Paolo Pandolfi
Beth Israel Deaconess Medical Center · USCancer Genetics (United States) · USBrigham and Women's Hospital · USBoston Biomedical Research Institute · USDana-Farber Cancer Institute · US

Funding

SPORE In Prostate CancerP50CA092629 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI JAMES A EASTHAM · 2001 to 2026
$63.0M
PTEN IN ONTOGENESIS AND TUMOR SUPPRESSIONR01CA082328 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI PANDOLFI, PIER PAOLO · 1999 to 2015
$5.3M
Role of POZ-zinc in hemopoietic malignaciesR01CA102142 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI PANDOLFI, PIER PAOLO · 2004 to 2014
$3.3M
CIHRNCI NIH HHS P50 CA092629NCI NIH HHS R01 CA082328NCI NIH HHS R01 CA102142NCI NIH HHS R01 CA-82328-0
6 · The paper itself

Abstract

PTEN (phosphatase and tensin homolog deleted on chromosome 10) is a tumor suppressor that antagonizes signaling through the phosphatidylinositol 3-kinase-Akt pathway. We have demonstrated that subtle decreases in PTEN abundance can have critical consequences for tumorigenesis. Here, we used a computational approach to identify miR-22, miR-25, and miR-302 as three PTEN-targeting microRNA (miRNA) families found within nine genomic loci. We showed that miR-22 and the miR-106b~25 cluster are aberrantly overexpressed in human prostate cancer, correlate with abundance of the miRNA processing enzyme DICER, and potentiate cellular transformation both in vitro and in vivo. We demonstrated that the intronic miR-106b~25 cluster cooperates with its host gene MCM7 in cellular transformation both in vitro and in vivo, so that the concomitant overexpression of MCM7 and the miRNA cluster triggers prostatic intraepithelial neoplasia in transgenic mice. Therefore, the MCM7 gene locus delivers two simultaneous oncogenic insults when amplified or overexpressed in human cancer. Thus, we have uncovered a proto-oncogenic miRNA-dependent network for PTEN regulation and defined the MCM7 locus as a critical factor in initiating prostate tumorigenesis.

Indexed as

Cell Transformation, NeoplasticIntronsMultigene FamilyProto-OncogenesAnimalsCell Cycle ProteinsDNA-Binding ProteinsHumansMaleMiceMice, TransgenicMicroRNAsMinichromosome Maintenance Complex Component 7Nuclear ProteinsProstatic NeoplasmsPTEN PhosphohydrolaseCell Cycle ProteinsDNA-Binding ProteinsMCM7 protein, humanMicroRNAsMinichromosome Maintenance Complex Component 7Nuclear ProteinsPTEN Phosphohydrolase

Identifiers

PMID20388916
PMCPMC2982149
OpenAlexW2078576279

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.