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Cells
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Myc Metabolism and Cancer
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Myc Metabolism and Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (10 March 2023) | Viewed by 5614

Special Issue Editor

Dr. Edward V. Prochownik

E-Mail Website
Guest Editor
1. Section of Hematology/Oncology, Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, PA, USA
2. The Department of Microbiology and Molecular Genetics, The University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
3. The Hillman Cancer Center, The University of Pittsburgh Medical Center, Pittsburgh, PA, USA
4. The University of Pittsburgh Liver Research Center, The University of Pittsburgh Medical Center, Pittsburgh, PA, USA
Interests: Myc proteins; cancer cell metabolism; cancer signaling pathways; tumor suppressors

Special Issue Information

Dear Colleagues,

This Special Issue of Cells will focus on the roles of the Myc oncoprotein and/or other members of the “Extended Myc Network” in regulating metabolism in normal and neoplastic cells. Both primary studies and reviews are welcome and should emphasize how these members control pathways that include, but are not limited to, glycolysis, glutaminolysis, fatty acid metabolism and mitochondrial structure and function. Articles that explore or review Myc-dependent connections between metabolism and energy-dependent processes such as the cell cycle and translation are of particular interest. Finally, the role of the Extended Myc Network in maintaining intracellular redox balance or promoting the function of tissues with critical roles in whole body metabolism such as the liver or pancreas are encouraged.

Dr. Edward V. Prochownik
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Myc
  • oncoprotein
  • metabolism
  • cancer

Published Papers (3 papers)

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Research

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29 pages, 7612 KiB  
Article
Disruption of Multiple Overlapping Functions Following Stepwise Inactivation of the Extended Myc Network
by Huabo Wang, Taylor Stevens, Jie Lu, Merlin Airik, Rannar Airik and Edward V. Prochownik
Cells 2022, 11(24), 4087; https://doi.org/10.3390/cells11244087 - 16 Dec 2022
Cited by 5 | Viewed by 1641
Abstract
Myc, a member of the “Myc Network” of bHLH-ZIP transcription factors, supervises proliferation, metabolism, and translation. It also engages in crosstalk with the related “Mlx Network” to co-regulate overlapping genes and functions. We investigated the consequences of stepwise conditional inactivation of Myc and [...] Read more.
Myc, a member of the “Myc Network” of bHLH-ZIP transcription factors, supervises proliferation, metabolism, and translation. It also engages in crosstalk with the related “Mlx Network” to co-regulate overlapping genes and functions. We investigated the consequences of stepwise conditional inactivation of Myc and Mlx in primary and SV40 T-antigen-immortalized murine embryonic fibroblasts (MEFs). Myc-knockout (MycKO) and Myc × Mlx “double KO” (DKO)—but not MlxKO—primary MEFs showed rapid growth arrest and displayed features of accelerated aging and senescence. However, DKO MEFs soon resumed proliferating, indicating that durable growth arrest requires an intact Mlx network. All three KO MEF groups deregulated multiple genes and functions pertaining to aging, senescence, and DNA damage recognition/repair. Immortalized KO MEFs proliferated in Myc’s absence while demonstrating variable degrees of widespread genomic instability and sensitivity to genotoxic agents. Finally, compared to primary MycKO MEFs, DKO MEFs selectively downregulated numerous gene sets associated with the p53 and retinoblastoma (Rb) pathways and G2/M arrest. Thus, the reversal of primary MycKO MEF growth arrest by either Mlx loss or SV40 T-antigen immortalization appears to involve inactivation of the p53 and/or Rb pathways. Full article
(This article belongs to the Special Issue Myc Metabolism and Cancer)
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Review

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25 pages, 1522 KiB  
Review
Rewired Metabolism Caused by the Oncogenic Deregulation of MYC as an Attractive Therapeutic Target in Cancers
by Laura Vízkeleti and Sándor Spisák
Cells 2023, 12(13), 1745; https://doi.org/10.3390/cells12131745 - 29 Jun 2023
Cited by 1 | Viewed by 1771
Abstract
MYC is one of the most deregulated oncogenes on multiple levels in cancer. As a node transcription factor, MYC plays a diverse regulatory role in many cellular processes, including cell cycle and metabolism, both in physiological and pathological conditions. The relentless growth and [...] Read more.
MYC is one of the most deregulated oncogenes on multiple levels in cancer. As a node transcription factor, MYC plays a diverse regulatory role in many cellular processes, including cell cycle and metabolism, both in physiological and pathological conditions. The relentless growth and proliferation of tumor cells lead to an insatiable demand for energy and nutrients, which requires the rewiring of cellular metabolism. As MYC can orchestrate all aspects of cellular metabolism, its altered regulation plays a central role in these processes, such as the Warburg effect, and is a well-established hallmark of cancer development. However, our current knowledge of MYC suggests that its spatial- and concentration-dependent contribution to tumorigenesis depends more on changes in the global or relative expression of target genes. As the direct targeting of MYC is proven to be challenging due to its relatively high toxicity, understanding its underlying regulatory mechanisms is essential for the development of tumor-selective targeted therapies. The aim of this review is to comprehensively summarize the diverse forms of MYC oncogenic deregulation, including DNA-, transcriptional- and post-translational level alterations, and their consequences for cellular metabolism. Furthermore, we also review the currently available and potentially attractive therapeutic options that exploit the vulnerability arising from the metabolic rearrangement of MYC-driven tumors. Full article
(This article belongs to the Special Issue Myc Metabolism and Cancer)
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25 pages, 1659 KiB  
Review
Regulation of Normal and Neoplastic Proliferation and Metabolism by the Extended Myc Network
by Edward V. Prochownik
Cells 2022, 11(24), 3974; https://doi.org/10.3390/cells11243974 - 8 Dec 2022
Cited by 7 | Viewed by 1855
Abstract
The Myc Network, comprising a small assemblage of bHLH-ZIP transcription factors, regulates many hundreds to thousands of genes involved in proliferation, energy metabolism, translation and other activities. A structurally and functionally related set of factors known as the Mlx Network also supervises some [...] Read more.
The Myc Network, comprising a small assemblage of bHLH-ZIP transcription factors, regulates many hundreds to thousands of genes involved in proliferation, energy metabolism, translation and other activities. A structurally and functionally related set of factors known as the Mlx Network also supervises some of these same functions via the regulation of a more limited but overlapping transcriptional repertoire. Target gene co-regulation by these two Networks is the result of their sharing of three members that suppress target gene expression as well as by the ability of both Network’s members to cross-bind one another’s consensus DNA sites. The two Networks also differ in that the Mlx Network’s control over transcription is positively regulated by several glycolytic pathway intermediates and other metabolites. These distinctive properties, functions and tissue expression patterns potentially allow for sensitive control of gene regulation in ways that are differentially responsive to environmental and metabolic cues while allowing for them to be both rapid and of limited duration. This review explores how such control might occur. It further discusses how the actual functional dependencies of the Myc and Mlx Networks rely upon cellular context and how they may differ between normal and neoplastic cells. Finally, consideration is given to how future studies may permit a more refined understanding of the functional interrelationships between the two Networks. Full article
(This article belongs to the Special Issue Myc Metabolism and Cancer)
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