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5.1
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Cells
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MYC Signaling in Cancer
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MYC Signaling in Cancer

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

Deadline for manuscript submissions: closed (1 July 2023) | Viewed by 8142

Special Issue Editor

Dr. Bernhard Zdársky

E-Mail Website
Guest Editor
Division Pharmacology, Karl Landsteiner University of Health Sciences, Dr.-Karl-Dorrek-Straße 30, 3500 Krems, Austria
Interests: acute myeloid leukemia; extracellular vesicles; JAK/STAT signaling; lymphoma; MYC; p53; STAT3

Special Issue Information

Dear Colleagues,

The protein family of MYC transcription factors orchestrates essential functions, including cell differentiation, proliferation, survival, apoptosis, and metabolism. In most human hematologic and solid tumor types, a deregulated expression of MYC proteins is recurrently found and often correlated with poor prognosis. There are multiple signaling pathways and numerous protein interactions that are known to regulate MYC activity, which further enables MYC to function as a potent oncoprotein. Despite its importance in tumorigenesis, MYC has remained an elusive therapeutic target and has for many years been considered undruggable. Significant progress has been achieved to date; however, further research is still of great importance to better understand the molecular mechanisms of MYC and the contribution of this oncoprotein to cancer development and progression. For this Special Issue of Cells, authors are invited to contribute both original research and review articles.

Dr. Bernhard Zdársky
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

  • cancer
  • MYC
  • oncoprotein
  • oncogene
  • transcription factor
  • tumorigenesis
  • tumor suppressor

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Published Papers (3 papers)

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Research

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21 pages, 5284 KiB  
Article
High Intrinsic Oncogenic Potential in the Myc-Box-Deficient Hydra Myc3 Protein
by Marion Lechable, Xuechen Tang, Stefan Siebert, Angelika Feldbacher, Monica L. Fernández-Quintero, Kathrin Breuker, Celina E. Juliano, Klaus R. Liedl, Bert Hobmayer and Markus Hartl
Cells 2023, 12(9), 1265; https://doi.org/10.3390/cells12091265 - 26 Apr 2023
Cited by 4 | Viewed by 2838
Abstract
The proto-oncogene myc has been intensively studied primarily in vertebrate cell culture systems. Myc transcription factors control fundamental cellular processes such as cell proliferation, cell cycle control and stem cell maintenance. Myc interacts with the Max protein and Myc/Max heterodimers regulate thousands of [...] Read more.
The proto-oncogene myc has been intensively studied primarily in vertebrate cell culture systems. Myc transcription factors control fundamental cellular processes such as cell proliferation, cell cycle control and stem cell maintenance. Myc interacts with the Max protein and Myc/Max heterodimers regulate thousands of target genes. The genome of the freshwater polyp Hydra encodes four myc genes (myc1-4). Previous structural and biochemical characterization showed that the Hydra Myc1 and Myc2 proteins share high similarities with vertebrate c-Myc, and their expression patterns suggested a function in adult stem cell maintenance. In contrast, an additional Hydra Myc protein termed Myc3 is highly divergent, lacking the common N-terminal domain and all conserved Myc-boxes. Single cell transcriptome analysis revealed that the myc3 gene is expressed in a distinct population of interstitial precursor cells committed to nerve- and gland-cell differentiation, where the Myc3 protein may counteract the stemness actions of Myc1 and Myc2 and thereby allow the implementation of a differentiation program. In vitro DNA binding studies showed that Myc3 dimerizes with Hydra Max, and this dimer efficiently binds to DNA containing the canonical Myc consensus motif (E-box). In vivo cell transformation assays in avian fibroblast cultures further revealed an unexpected high potential for oncogenic transformation in the conserved Myc3 C-terminus, as compared to Hydra Myc2 or Myc1. Structure modeling of the Myc3 protein predicted conserved amino acid residues in its bHLH-LZ domain engaged in Myc3/Max dimerization. Mutating these amino acid residues in the human c-Myc (MYC) sequence resulted in a significant decrease in its cell transformation potential. We discuss our findings in the context of oncogenic transformation and cell differentiation, both relevant for human cancer, where Myc represents a major driver. Full article
(This article belongs to the Special Issue MYC Signaling in Cancer)
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13 pages, 2045 KiB  
Article
Tumor Growth Remains Refractory to Myc Ablation in Host Macrophages
by Riley J. Morrow, Amr H. Allam, Josh Konecnik, David Baloyan, Christine Dijkstra, Moritz F. Eissmann, Saumya P. Jacob, Megan O’Brien, Ashleigh R. Poh and Matthias Ernst
Cells 2022, 11(24), 4104; https://doi.org/10.3390/cells11244104 - 17 Dec 2022
Viewed by 2149
Abstract
Aberrant expression of the oncoprotein c-Myc (Myc) is frequently observed in solid tumors and is associated with reduced overall survival. In addition to well-recognized cancer cell-intrinsic roles of Myc, studies have also suggested tumor-promoting roles for Myc in cells of the tumor microenvironment, [...] Read more.
Aberrant expression of the oncoprotein c-Myc (Myc) is frequently observed in solid tumors and is associated with reduced overall survival. In addition to well-recognized cancer cell-intrinsic roles of Myc, studies have also suggested tumor-promoting roles for Myc in cells of the tumor microenvironment, including macrophages and other myeloid cells. Here, we benchmark Myc inactivation in tumor cells against the contribution of its expression in myeloid cells of murine hosts that harbor endogenous or allograft tumors. Surprisingly, we observe that LysMCre-mediated Myc ablation in host macrophages does not attenuate tumor growth regardless of immunogenicity, the cellular origin of the tumor, the site it develops, or the stage along the tumor progression cascade. Likewise, we find no evidence for Myc ablation to revert or antagonize the polarization of alternatively activated immunosuppressive macrophages. Thus, we surmise that systemic targeting of Myc activity may confer therapeutic benefits primarily through limiting Myc activity in tumor cells rather than reinvigorating the anti-tumor activity of macrophages. Full article
(This article belongs to the Special Issue MYC Signaling in Cancer)
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Review

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28 pages, 2936 KiB  
Review
Lessons from Using Genetically Engineered Mouse Models of MYC-Induced Lymphoma
by René Winkler, Eva-Maria Piskor and Christian Kosan
Cells 2023, 12(1), 37; https://doi.org/10.3390/cells12010037 - 22 Dec 2022
Cited by 1 | Viewed by 2380
Abstract
Oncogenic overexpression of MYC leads to the fatal deregulation of signaling pathways, cellular metabolism, and cell growth. MYC rearrangements are found frequently among non-Hodgkin B-cell lymphomas enforcing MYC overexpression. Genetically engineered mouse models (GEMMs) were developed to understand MYC-induced B-cell lymphomagenesis. Here, we [...] Read more.
Oncogenic overexpression of MYC leads to the fatal deregulation of signaling pathways, cellular metabolism, and cell growth. MYC rearrangements are found frequently among non-Hodgkin B-cell lymphomas enforcing MYC overexpression. Genetically engineered mouse models (GEMMs) were developed to understand MYC-induced B-cell lymphomagenesis. Here, we highlight the advantages of using Eµ-Myc transgenic mice. We thoroughly compiled the available literature to discuss common challenges when using such mouse models. Furthermore, we give an overview of pathways affected by MYC based on knowledge gained from the use of GEMMs. We identified top regulators of MYC-induced lymphomagenesis, including some candidates that are not pharmacologically targeted yet. Full article
(This article belongs to the Special Issue MYC Signaling in Cancer)
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