Evidence map›Paper›PMID 26676759›Full record

ArticleCancer research2016

Myc Induces miRNA-Mediated Apoptosis in Response to HDAC Inhibition in Hematologic Malignancies.

Clare M Adams, Scott W Hiebert, Christine M Eischen

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2016. 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 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.4field-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

38 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  8. Review
  9. Function of BCLAF1 in human disease.Oncology letters · 2022
    Review
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  11. Review
  12. Article
  13. Article
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  16. Article
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  18. Article
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  20. The Roles of Histone Deacetylases and Their Inhibitors in Cancer Therapy.Frontiers in cell and developmental biology · 2020
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Clare M AdamsDepartment of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.
Scott W HiebertDepartment of Biochemistry, Vanderbilt University Medical Center, Nashville, Tennessee.
Christine M EischenDepartment of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee. christine.eischen@vanderbilt.edu.
Vanderbilt University Medical Center · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
TRAINING PROGRAM IN CELLULAR, BIOCHEMICAL, &MOLECULAR ST32GM008554 · NIGMS · VANDERBILT UNIVERSITY · PI PATTON, JAMES G. · 1995 to 2020
$7.4M
Role of AML1-ETO in Acute LeukemiaR01CA064140 · NCI · VANDERBILT UNIVERSITY · PI HIEBERT, SCOTT W · 1994 to 2018
$5.7M
Hdac3 as a therapeutic target in BCL6-dependent lymphomaR01CA164605 · NCI · VANDERBILT UNIVERSITY · PI HIEBERT, SCOTT W · 2012 to 2022
$3.9M
Regulation of transcription and tumor suppression by MTG family membersR01CA178030 · NCI · VANDERBILT UNIVERSITY · PI HIEBERT, SCOTT W · 2014 to 2018
$1.8M
Regulation of Myc-Mediated TumorigenesisR01CA148950 · NCI · VANDERBILT UNIVERSITY · PI EISCHEN, CHRISTINE M. · 2011 to 2015
$1.7M
Novel Mechanism for Myc-Induced ApoptosisF31CA165728 · NCI · VANDERBILT UNIVERSITY · PI ADAMS, CLARE MARIE · 2012 to 2014
$80k
NCI NIH HHS F31 CA165728NCI NIH HHS F31CA165728NCI NIH HHS P30 CA068485NCI NIH HHS P30CA068485NCI NIH HHS R01 CA064140NCI NIH HHS R01 CA148950NCI NIH HHS R01CA148950NCI NIH HHS R01 CA164605NCI NIH HHS R01 CA178030NCI NIH HHS R01CA178030NIGMS NIH HHS T32 GM008554NIGMS NIH HHS T32GM08554
6 · The paper itself

Abstract

Alterations in the expression or function of histone deacetylases (HDAC) contribute to the development and progression of hematologic malignancies. Consequently, the development and implementation of HDAC inhibitors has proven to be therapeutically beneficial, particularly for hematologic malignancies. However, the molecular mechanisms by which HDAC inhibition (HDACi) induces tumor cell death remain unresolved. Here, we investigated the effects of HDACi in Myc-driven B-cell lymphoma and five other hematopoietic malignancies. We determined that Myc-mediated transcriptional repression of the miR-15 and let-7 families in malignant cells was relieved upon HDACi, and Myc was required for their upregulation. The miR-15 and let-7 families then targeted and downregulated the antiapoptotic genes Bcl-2 and Bcl-xL, respectively, to induce HDACi-mediated apoptosis. Notably, Myc also transcriptionally upregulated these miRNA in untransformed cells, indicating that this Myc-induced miRNA-mediated apoptotic pathway is suppressed in malignant cells, but becomes reactivated upon HDACi. Taken together, our results reveal a previously unknown mechanism by which Myc induces apoptosis independent of the p53 pathway and as a response to HDACi in malignant hematopoietic cells.

Indexed as

AnimalsApoptosisCell Line, TumorHematologic NeoplasmsHistone Deacetylase InhibitorsHumansMice, Inbred C57BLMicroRNAsProto-Oncogene Proteins c-mycTransfectionHistone Deacetylase InhibitorsMicroRNAsProto-Oncogene Proteins c-myc

Identifiers

PMID26676759
PMCPMC4738141
OpenAlexW2263311874

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.