Evidence map›Paper›PMID 24968297›Full record

ArticlePloS one2014

MicroRNA 17-92 cluster mediates ETS1 and ETS2-dependent RAS-oncogenic transformation.

Mohamed Kabbout, Duaa Dakhlallah, Sudarshana Sharma, Agnieszka Bronisz, Ruchika Srinivasan, Melissa Piper, Clay B Marsh, Michael C Ostrowski

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. ETS‑1/ETS‑2 transcription factors in CVD (Review).International journal of molecular medicine · 2026
    Review
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  12. ETS-targeted therapy: can it substitute for MEK inhibitors?Clinical and translational medicine · 2017
    Review
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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

8 authors at 1 institution in 1 country.

Mohamed KabboutDepartment of Molecular and Cellular Biochemistry, College of Medicine, The Ohio State University, Columbus, Ohio, United States of America; Graduate Program in Molecular Cellular and Developmental Biology, The Ohio State University, Columbus, Ohio, United States of America; Solid Tumor Program, Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, United States of America.
Duaa DakhlallahGraduate Program in Molecular Cellular and Developmental Biology, The Ohio State University, Columbus, Ohio, United States of America; Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States of America.
Sudarshana SharmaDepartment of Molecular and Cellular Biochemistry, College of Medicine, The Ohio State University, Columbus, Ohio, United States of America; Solid Tumor Program, Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, United States of America.
Agnieszka BroniszDepartment of Molecular and Cellular Biochemistry, College of Medicine, The Ohio State University, Columbus, Ohio, United States of America; Solid Tumor Program, Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, United States of America.
Ruchika SrinivasanDepartment of Molecular and Cellular Biochemistry, College of Medicine, The Ohio State University, Columbus, Ohio, United States of America; Graduate Program in Molecular Cellular and Developmental Biology, The Ohio State University, Columbus, Ohio, United States of America; Solid Tumor Program, Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, United States of America.
Melissa PiperDorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States of America; Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Internal Medicine, College of Medicine, The Ohio State University, Columbus, Ohio, United States of America.
Clay B MarshDorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States of America; Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Internal Medicine, College of Medicine, The Ohio State University, Columbus, Ohio, United States of America.
Michael C OstrowskiDepartment of Molecular and Cellular Biochemistry, College of Medicine, The Ohio State University, Columbus, Ohio, United States of America; Solid Tumor Program, Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, United States of America.
The Ohio State University · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Jennifer A. Woyach · 1985 to 2026
$132.3M
Suppression of Mammary Tumorigenesis by Stromal p53P01CA097189 · NCI · OHIO STATE UNIVERSITY · PI ROSOL, THOMAS J · 2004 to 2016
$16.1M
RAS ONCOGENE-ACTIVATED GENE EXPRESSIONR01CA053271 · NCI · OHIO STATE UNIVERSITY · PI OSTROWSKI, MICHAEL C. · 1991 to 2011
$2.9M
NCI NIH HHS P01 CA097189NCI NIH HHS P01CA097189NCI NIH HHS P30 CA016058NCI NIH HHS R01 CA053271NCI NIH HHS R01CA053271
6 · The paper itself

Abstract

The ETS-family transcription factors Ets1 and Ets2 are evolutionarily conserved effectors of the RAS/ERK signaling pathway, but their function in Ras cellular transformation and biology remains unclear. Taking advantage of Ets1 and Ets2 mouse models to generate Ets1/Ets2 double knockout mouse embryonic fibroblasts, we demonstrate that deletion of both Ets1 and Ets2 was necessary to inhibit HrasG12V induced transformation both in vitro and in vivo. HrasG12V expression in mouse embryonic fibroblasts increased ETS1 and ETS2 expression and binding to cis-regulatory elements on the c-Myc proximal promoter, and consequently induced a robust increase in MYC expression. The expression of the oncogenic microRNA 17-92 cluster was increased in HrasG12V transformed cells, but was significantly reduced when ETS1 and ETS2 were absent. MYC and ETS1 or ETS2 collaborated to increase expression of the oncogenic microRNA 17-92 cluster in HrasG12V transformed cells. Enforced expression of exogenous MYC or microRNA 17-92 rescued HrasG12V transformation in Ets1/Ets2-null cells, revealing a direct function for MYC and microRNA 17-92 in ETS1/ETS2-dependent HrasG12V transformation.

Indexed as

CarcinogenesisCell Transformation, NeoplasticAnimalsCell LineFibroblastsGene Knockout TechniquesHumansMaleMiceMicroRNAsOncogene Protein p21(ras)Proto-Oncogene Protein c-ets-1Proto-Oncogene Protein c-ets-2Proto-Oncogene Proteins c-mycMicroRNAsOncogene Protein p21(ras)Proto-Oncogene Protein c-ets-1Proto-Oncogene Protein c-ets-2Proto-Oncogene Proteins c-myc

Identifiers

PMID24968297
PMCPMC4072627
OpenAlexW1983314269

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.