Regulation of cancer cell metabolism: oncogenic MYC in the driver’s seat

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Abstract

Cancer cells must rewire cellular metabolism to satisfy the demands of unbridled growth and proliferation. As such, most human cancers differ from normal counterpart tissues by a plethora of energetic and metabolic reprogramming. Transcription factors of the MYC family are deregulated in up to 70% of all human cancers through a variety of mechanisms. Oncogenic levels of MYC regulates almost every aspect of cellular metabolism, a recently revisited hallmark of cancer development. Meanwhile, unrestrained growth in response to oncogenic MYC expression creates dependency on MYC-driven metabolic pathways, which in principle provides novel targets for development of effective cancer therapeutics. In the current review, we summarize the significant progress made toward understanding how MYC deregulation fuels metabolic rewiring in malignant transformation.

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Targeting oncogenic Myc as a strategy for cancer treatment

Hui Chen, Hudan Liu, Guoliang Qing (2018)

The MYC family oncogene is deregulated in >50% of human cancers, and this deregulation is frequently associated with poor prognosis and unfavorable patient survival. Myc has a central role in almost every aspect of the oncogenic process, orchestrating proliferation, apoptosis, differentiation, and metabolism. Although Myc inhibition would be a powerful approach for the treatment of many types of cancers, direct targeting of Myc has been a challenge for decades owing to its “undruggable” protein structure. Hence, alternatives to Myc blockade have been widely explored to achieve desirable anti-tumor effects, including Myc/Max complex disruption, MYC transcription and/or translation inhibition, and Myc destabilization as well as the synthetic lethality associated with Myc overexpression. In this review, we summarize the latest advances in targeting oncogenic Myc, particularly for cancer therapeutic purposes.

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Author and article information

Contributors

Guoliang Qing: qingguoliang@whu.edu.cn

Journal

Journal ID (nlm-ta): Signal Transduct Target Ther

Journal ID (iso-abbrev): Signal Transduct Target Ther

Title: Signal Transduction and Targeted Therapy

Publisher: Nature Publishing Group UK (London )

ISSN (Print): 2095-9907

ISSN (Electronic): 2059-3635

Publication date (Electronic): 10 July 2020

Publication date PMC-release: 10 July 2020

Publication date Collection: 2020

Volume: 5

Electronic Location Identifier: 124

Affiliations

[1 ]GRID grid.413247.7, Department of Urology, , Zhongnan Hospital of Wuhan University, ; Wuhan, 430071 China

[2 ]GRID grid.49470.3e, ISNI 0000 0001 2331 6153, Frontier Science Center for Immunology & Metabolism, Medical Research Institute, , Wuhan University, ; Wuhan, 430071 China

Author information

Hudan Liu http://orcid.org/0000-0003-1362-6048

Article

Publisher ID: 235

DOI: 10.1038/s41392-020-00235-2

PMC ID: 7351732

PubMed ID: 32651356

SO-VID: 2a254f31-4684-44d9-b2c3-103fa0ca11c7

License:

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

History

Date received : 20 April 2020

Date revision received : 11 June 2020

Date accepted : 15 June 2020

Funding

Funded by: FundRef https://doi.org/10.13039/501100001809, National Natural Science Foundation of China (National Science Foundation of China);

Award ID: 81830084

Award Recipient : Guoliang Qing

Funded by: National Science Fund for Distinguished Young Scholars (Grant 81725013 to G.Q.); National Natural Science Foundation of China (Grant 81830084 to G.Q); Medical Science Advancement Program (Basic Medical Sciences) of Wuhan University (Grant TFJC2018005 to G.Q.).