Evidence map›Paper›PMID 26749280›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

MicroRNA-378-mediated suppression of Runx1 alleviates the aggressive phenotype of triple-negative MDA-MB-231 human breast cancer cells.

Gillian Browne, Julie A Dragon, Deli Hong, Terri L Messier, Jonathan A R Gordon, Nicholas H Farina, Joseph R Boyd, Jennifer J VanOudenhove, Andrew W Perez, Sayyed K Zaidi and 3 more

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

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
2.7field-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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

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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

13 authors at 1 institution in 1 country.

Gillian BrowneDepartment of Biochemistry & University of Vermont Cancer Center, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, VT, 05405, USA.
Julie A DragonDepartment of Microbiology and Molecular Genetics, University of Vermont, 95 Carrigan Avenue, Burlington, VT, 05405, USA.
Deli HongDepartment of Biochemistry & University of Vermont Cancer Center, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, VT, 05405, USA.
Terri L MessierDepartment of Biochemistry & University of Vermont Cancer Center, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, VT, 05405, USA.
Jonathan A R GordonDepartment of Biochemistry & University of Vermont Cancer Center, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, VT, 05405, USA.
Nicholas H FarinaDepartment of Biochemistry & University of Vermont Cancer Center, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, VT, 05405, USA.
Joseph R BoydDepartment of Biochemistry & University of Vermont Cancer Center, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, VT, 05405, USA.
Jennifer J VanOudenhoveDepartment of Biochemistry & University of Vermont Cancer Center, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, VT, 05405, USA.
Andrew W PerezDepartment of Biochemistry & University of Vermont Cancer Center, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, VT, 05405, USA.
Sayyed K ZaidiDepartment of Biochemistry & University of Vermont Cancer Center, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, VT, 05405, USA.
Janet L SteinDepartment of Biochemistry & University of Vermont Cancer Center, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, VT, 05405, USA.
Gary S SteinDepartment of Biochemistry & University of Vermont Cancer Center, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, VT, 05405, USA.
Jane B LianDepartment of Biochemistry & University of Vermont Cancer Center, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, VT, 05405, USA. jane.lian@uvm.edu.
University of Vermont · US

Funding

Vermont INBRE Administrative Supplement 2024 AWD 118P20GM103449 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI Julie Dragon · 2012 to 2026
$58.4M
SUBNUCLEAR TARGETING OF TRANSCRIPTION FACTORSP01CA082834 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI STEIN, GARY S. · 2001 to 2015
$18.4M
CONTROL OF OSTEOBLAST PROLIFERATION AND DIFFERENTIATIONR01AR039588 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LIAN, JANE B., STEIN, GARY S. · 1990 to 2019
$8.0M
Synthesis of Osteocalcin in BoneR37DE012528 · NIDCR · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LIAN, JANE B. · 2008 to 2017
$5.0M
Deregulated microRNAs in Acute Myeloid LeukemiaR03CA167726 · NCI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI ZAIDI, SAYYED KALEEM · 2013 to 2014
$150k
NCI NIH HHS P01 CA082834NCI NIH HHS R03 CA167726NIAMS NIH HHS R01 AR039588NIDCR NIH HHS R37 DE012528NIGMS NIH HHS P20 GM103449
6 · The paper itself

Abstract

The Runx1 transcription factor, known for its essential role in normal hematopoiesis, was reported in limited studies to be mutated or associated with human breast tumor tissues. Runx1 increases concomitantly with disease progression in the MMTV-PyMT transgenic mouse model of breast cancer. Compelling questions relate to mechanisms that regulate Runx1 expression in breast cancer. Here, we tested the hypothesis that dysregulation of Runx1-targeting microRNAs (miRNAs) allows for pathologic increase of Runx1 during breast cancer progression. Microarray profiling of the MMTV-PyMT model revealed significant downregulation of numerous miRNAs predicted to target Runx1. One of these, miR-378, was inversely correlated with Runx1 expression during breast cancer progression in mice and in human breast cancer cell lines MCF7 and triple-negative MDA-MB-231 that represent early- and late-stage diseases, respectively. MiR-378 is nearly absent in MDA-MB-231 cells. Luciferase reporter assays revealed that miR-378 binds the Runx1 3' untranslated region (3'UTR) and inhibits Runx1 expression. Functionally, we demonstrated that ectopic expression of miR-378 in MDA-MB-231 cells inhibited Runx1 and suppressed migration and invasion, while inhibition of miR-378 in MCF7 cells increased Runx1 levels and cell migration. Depletion of Runx1 in late-stage breast cancer cells resulted in increased expression of both the miR-378 host gene PPARGC1B and pre-miR-378, suggesting a feedback loop. Taken together, our study identifies a novel and clinically relevant mechanism for regulation of Runx1 in breast cancer that is mediated by a PPARGC1B-miR-378-Runx1 regulatory pathway. Our results highlight the translational potential of miRNA replacement therapy for inhibiting Runx1 in breast cancer.

Indexed as

3' Untranslated RegionsAnimalsCell Line, TumorCell MovementCore Binding Factor Alpha 2 SubunitDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMiceMicroRNAsPhenotypeTriple Negative Breast Neoplasms3' Untranslated RegionsCore Binding Factor Alpha 2 SubunitMicroRNAsBreast cancerInvasionMigrationMiR-378MMTV-PyMTRunx1

Identifiers

PMID26749280
PMCPMC4939137
OpenAlexW2223490153

What Socratic 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 Socratic graph.