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Trends Cell Biol. 2015 Apr;25(4):241-8. doi: 10.1016/j.tcb.2014.10.006. Epub 2014 Dec 1.

Taming of the beast: shaping Myc-dependent amplification.

Author information

1
Theodor Boveri Institute, Biocenter, and Comprehensive Cancer Center, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
2
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA. Electronic address: Charles_lin@dfci.harvard.edu.
3
Theodor Boveri Institute, Biocenter, and Comprehensive Cancer Center, University of Würzburg, Am Hubland, 97074 Würzburg, Germany. Electronic address: martin.eilers@biozentrum.uni-wuerzburg.de.
4
Laboratory of Pathology, 10 Center Drive, Bethesda, MD 20892-1500, USA. Electronic address: levens@helix.nih.gov.

Abstract

Myc deregulation is a hallmark oncogenic event where overexpression of the transcription factor gives rise to numerous tumorigenic phenotypes. The complex consequences of Myc deregulation have prevented clear mechanistic interpretations of its function. A synthesis of recent experimental observations offers a consensus on the direct transcriptional function of Myc: when overexpressed, Myc broadly engages the established euchromatic cis-regulatory landscape of the cell, where the factor generally amplifies transcription. The level of Myc binding at target genes and the transcriptional output are differentially modulated by additional regulators, including Miz1. Targeting Myc oncogenic activity will require an understanding of whether amplification promotes tumorigenesis and the consequences of amplification in tumors adapted to oncogenic Myc.

KEYWORDS:

Myc; cancer; transcription

PMID:
25475704
PMCID:
PMC4380620
DOI:
10.1016/j.tcb.2014.10.006
[Indexed for MEDLINE]
Free PMC Article

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