Next Article in Journal / Special Issue
Role of MYC in B Cell Lymphomagenesis
Previous Article in Journal / Special Issue
The MYCN Protein in Health and Disease
Open AccessReview

Targeting MYC Dependence by Metabolic Inhibitors in Cancer

Department of Pediatrics, Division of Hematology/Oncology/BMT & Aflac Cancer and Blood Disorders Center, Emory University School of Medicine, 1760 Haygood Drive NE, HSRB E308, Atlanta, GA 30322, USA
Author to whom correspondence should be addressed.
Genes 2017, 8(4), 114;
Received: 6 January 2017 / Revised: 23 March 2017 / Accepted: 27 March 2017 / Published: 31 March 2017
(This article belongs to the Special Issue MYC Networks)
PDF [526 KB, uploaded 7 April 2017]


Abstract: MYC is a critical growth regulatory gene that is commonly overexpressed in a wide range of cancers. Therapeutic targeting of MYC transcriptional activity has long been a goal, but it has been difficult to achieve with drugs that directly block its DNA-binding ability. Additional approaches that exploit oncogene addiction are promising strategies against MYC-driven cancers. Also, drugs that target metabolic regulatory pathways and enzymes have potential for indirectly reducing MYC levels. Glucose metabolism and oxidative phosphorylation, which can be targeted by multiple agents, promote cell growth and MYC expression. Likewise, modulation of the signaling pathways and protein synthesis regulated by adenosine monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR) can also be an effective route for suppressing MYC translation. Furthermore, recent data suggest that metabolism of nucleotides, fatty acids and glutamine are exploited to alter MYC levels. Combination therapies offer potential new approaches to overcome metabolic plasticity caused by single agents. Although potential toxicities must be carefully controlled, new inhibitors currently being tested in clinical trials offer significant promise. Therefore, as both a downstream target of metabolism and an upstream regulator, MYC is a prominent central regulator of cancer metabolism. Exploiting metabolic vulnerabilities of MYC-driven cancers is an emerging research area with translational potential. View Full-Text
Keywords: transcription factor; metabolism; cancer; signal transduction; combination therapy transcription factor; metabolism; cancer; signal transduction; combination therapy

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Sabnis, H.S.; Somasagara, R.R.; Bunting, K.D. Targeting MYC Dependence by Metabolic Inhibitors in Cancer. Genes 2017, 8, 114.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Genes EISSN 2073-4425 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top