Evidence map›Paper›PMID 28415794›Full record

ArticleOncotarget2017

MicroRNAs of the mir-17~92 cluster regulate multiple aspects of pancreatic tumor development and progression.

Brian Quattrochi, Anushree Gulvady, David R Driscoll, Makoto Sano, David S Klimstra, Christopher E Turner, Brian C Lewis

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
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

7 authors at 4 institutions in 2 countries.

Brian QuattrochiDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Anushree GulvadyDepartment of Cell and Developmental Biology, State University of New York Upstate Medical Center, Syracuse, NY 13210, USA.
David R DriscollDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Makoto SanoDivision of Pathology, Department of Pathology and Microbiology, Nihon University School of Medicine, Itabashi-ku, Tokyo, 173-8610, Japan.
David S KlimstraDepartment of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
Christopher E TurnerDepartment of Cell and Developmental Biology, State University of New York Upstate Medical Center, Syracuse, NY 13210, USA.
Brian C LewisDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
University of Massachusetts Chan Medical School · USSUNY Upstate Medical University · USMemorial Sloan Kettering Cancer Center · USNihon University · JP

Funding

Paxillin and Hic-5 in Coordination of Cancer Cell Invasion MechanismsR01CA163296 · NCI · UPSTATE MEDICAL UNIVERSITY · PI TURNER, CHRISTOPHER E · 2012 to 2016
$1.6M
Roles of MiR-17-92 Cluster MicroRNAs in K-Ras-Induced Pancreatic TumorigenesisF30CA168063 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI QUATTROCHI, BRIAN JOSEPH · 2012 to 2015
$116k
NCI NIH HHS F30 CA168063NCI NIH HHS R01 CA163296
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy characterized by resistance to currently employed chemotherapeutic approaches. Members of the mir-17~92 cluster of microRNAs (miRNAs) are upregulated in PDAC, but the precise roles of these miRNAs in PDAC are unknown. Using genetically engineered mouse models, we show that loss of mir-17~92 reduces ERK pathway activation downstream of mutant KRAS and promotes the regression of KRASG12D-driven precursor pancreatic intraepithelial neoplasias (PanINs) and their replacement by normal exocrine tissue. In a PDAC model driven by concomitant KRASG12D expression and Trp53 heterozygosity, mir-17~92 deficiency extended the survival of mice that lacked distant metastasis. Moreover, mir-17~92-deficient PDAC cell lines display reduced invasion activity in transwell assays, form fewer invadopodia rosettes than mir-17~92-competent cell lines and are less able to degrade extracellular matrix. Specific inhibition of miR-19 family miRNAs with antagomirs recapitulates these phenotypes, suggesting that miR-19 family miRNAs are important mediators of PDAC cell invasion. Together these data demonstrate an oncogenic role for mir-17~92 at multiple stages of pancreatic tumorigenesis and progression; specifically, they link this miRNA cluster to ERK pathway activation and precursor lesion maintenance in vivo and identify a novel role for miR-19 family miRNAs in promoting cancer cell invasion.

Indexed as

Multigene FamilyAge FactorsAllelesAnimalsCarcinoma, Intraductal, NoninfiltratingCarcinoma, Pancreatic DuctalCell Line, TumorCell Transformation, NeoplasticDisease ProgressionGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockout TechniquesHumansMAP Kinase Signaling SystemMiceMice, TransgenicMicroRNAsinvasionmir-17~92pancreatic cancerPanINregression

Identifiers

PMID28415794
PMCPMC5482626
OpenAlexW2597264667

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.