Evidence map›Paper›PMID 25117713›Full record

ArticleCancer cell2014

MYC through miR-17-92 suppresses specific target genes to maintain survival, autonomous proliferation, and a neoplastic state.

Yulin Li, Peter S Choi, Stephanie C Casey, David L Dill, Dean W Felsher

Open access · bronzeAbstract read
In one paragraph

Article in Cancer cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

116 citing papers in PubMed, 171 citations in OpenAlex.

  1. Article
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  9. mInternational journal of oral science · 2024
    Article
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  13. Article
  14. Article
  15. Science (New York, N.Y.) · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. The SUV4-20H Histone Methyltransferases in Health and Disease.International journal of molecular sciences · 2022
    Review
  20. Article

56 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Yulin LiDivision of Oncology, Department of Medicine and Pathology, Stanford University, Stanford, CA 94305, USA.
Peter S ChoiDivision of Oncology, Department of Medicine and Pathology, Stanford University, Stanford, CA 94305, USA.
Stephanie C CaseyDivision of Oncology, Department of Medicine and Pathology, Stanford University, Stanford, CA 94305, USA.
David L DillDepartment of Computer Science, Stanford University, Stanford, CA 94305, USA.
Dean W FelsherDivision of Oncology, Department of Medicine and Pathology, Stanford University, Stanford, CA 94305, USA. Electronic address: dfelsher@stanford.edu.
Stanford University · US

Funding

TRANS-NETWORK PROJECTSU54CA143907 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GROSS, MITCHELL E · 2009 to 2013
$15.2M
MODELING THE ROLE OF PROGRESSION IN FOLLICULAR LYMPHOMAU54CA149145 · NCI · STANFORD UNIVERSITY · PI PLEVRITIS, SYLVIA KATINA · 2010 to 2014
$12.1M
Modeling and Predicting Therapeutic Resistance of CancerU01CA188383 · NCI · STANFORD UNIVERSITY · PI FELSHER, DEAN W, GAMBHIR, SANJIV S · 2014 to 2018
$3.2M
Mechanisms by which Oncogene Inactivation Elicits Tumor Cell DeathR01CA170378 · NCI · STANFORD UNIVERSITY · PI FELSHER, DEAN W · 2012 to 2015
$2.1M
The Role of CD4+ T Cells in Oncogene AddictionF32CA177139 · NCI · STANFORD UNIVERSITY · PI CASEY, STEPHANIE CATHERINE · 2013 to 2014
$102k
NCI NIH HHS 1F32CA177139NCI NIH HHS F32 CA177139NCI NIH HHS R01 CA170378NCI NIH HHS R01CA170378NCI NIH HHS U01 CA188383NCI NIH HHS U54 CA143907NCI NIH HHS U54CA143907NCI NIH HHS U54 CA149145NCI NIH HHS U54CA149145PHS HHS 5T32A107290
6 · The paper itself

Abstract

The MYC oncogene regulates gene expression through multiple mechanisms, and its overexpression culminates in tumorigenesis. MYC inactivation reverses turmorigenesis through the loss of distinguishing features of cancer, including autonomous proliferation and survival. Here we report that MYC via miR-17-92 maintains a neoplastic state through the suppression of chromatin regulatory genes Sin3b, Hbp1, Suv420h1, and Btg1, as well as the apoptosis regulator Bim. The enforced expression of miR-17-92 prevents MYC suppression from inducing proliferative arrest, senescence, and apoptosis and abrogates sustained tumor regression. Knockdown of the five miR-17-92 target genes blocks senescence and apoptosis while it modestly delays proliferative arrest, thus partially recapitulating miR-17-92 function. We conclude that MYC, via miR-17-92, maintains a neoplastic state by suppressing specific target genes.

Indexed as

Cell ProliferationCell SurvivalAnimalsApoptosisGene Expression Regulation, NeoplasticLymphomaMiceMicroRNAsMultigene FamilyNeoplasm TransplantationProto-Oncogene Proteins c-mycRNA InterferenceTumor BurdenTumor Cells, CulturedMicroRNAsMIRN17-92 microRNA, mouseMyc protein, mouseProto-Oncogene Proteins c-myc

Identifiers

PMID25117713
PMCPMC4191901
OpenAlexW2065397600

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.