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MYC and p53 Gene Families
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MYC and p53 Gene Families

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 2588

Special Issue Editor

Dr. Yusuke Suenaga

E-Mail Website
Guest Editor
Department of Molecular Carcinogenesis, Chiba Cancer Center Research Institute, Chiba 260-0801, Japan
Interests: neuroblastoma; brain tumor; transcriptional regulation; gene evolution; de novo gene; long non-coding RNA; p53 family members; MYC family members

Special Issue Information

Dear Colleagues,

MYC and p53 are a representative oncogene and tumor suppressor gene, respectively. Both genes comprise a family of genes and the two families regulate each other's functions in cancer, resulting in a fierce competition between tumor promotion and suppression. The two gene families regulate each other directly and indirectly not only in cancer, but also in development and ageing, influencing the phenotype of the individual throughout life. This special issue calls for original articles and reviews focusing on the biological roles of the p53 and MYC gene families.

The following are examples of research topics of interest; however, any related studies regarding the biological roles of the p53 gene family (p53, p63, and p73) and MYC gene family (MYC, MYCN, and MYCL) will be considered.

  1. The role of the p53 family of genes (p53, p63, and p73) or their downstream target genes in cancer, development, and ageing.
  2. The role of MYC family of genes (MYC, MYCN, and MYCL) or their downstream target genes in cancer, development, and ageing.
  3. Inter-regulatory relationship between members of the p53 and MYC gene families.
  4. Evolutionary studies on the p53 or MYC gene families.

Dr. Yusuke Suenaga
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

Published Papers (2 papers)

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Research

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10 pages, 656 KiB  
Article
DNA Ligase 4 Contributes to Cell Proliferation against DNA-PK Inhibition in MYCN-Amplified Neuroblastoma IMR32 Cells
by Kiyohiro Ando, Yusuke Suenaga and Takehiko Kamijo
Int. J. Mol. Sci. 2023, 24(10), 9012; https://doi.org/10.3390/ijms24109012 - 19 May 2023
Viewed by 1363
Abstract
Identifying the vulnerability of altered DNA repair machinery that displays synthetic lethality with MYCN amplification is a therapeutic rationale in unfavourable neuroblastoma. However, none of the inhibitors for DNA repair proteins are established as standard therapy in neuroblastoma. Here, we investigated whether DNA-PK [...] Read more.
Identifying the vulnerability of altered DNA repair machinery that displays synthetic lethality with MYCN amplification is a therapeutic rationale in unfavourable neuroblastoma. However, none of the inhibitors for DNA repair proteins are established as standard therapy in neuroblastoma. Here, we investigated whether DNA-PK inhibitor (DNA-PKi) could inhibit the proliferation of spheroids derived from neuroblastomas of MYCN transgenic mice and MYCN-amplified neuroblastoma cell lines. DNA-PKi exhibited an inhibitory effect on the proliferation of MYCN-driven neuroblastoma spheroids, whereas variable sensitivity was observed in those cell lines. Among them, the accelerated proliferation of IMR32 cells was dependent on DNA ligase 4 (LIG4), which comprises the canonical non-homologous end-joining pathway of DNA repair. Notably, LIG4 was identified as one of the worst prognostic factors in patients with MYCN-amplified neuroblastomas. It may play complementary roles in DNA-PK deficiency, suggesting the therapeutic potential of LIG4 inhibition in combination with DNA-PKi for MYCN-amplified neuroblastomas to overcome resistance to multimodal therapy. Full article
(This article belongs to the Special Issue MYC and p53 Gene Families)
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Review

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17 pages, 1343 KiB  
Review
Isoform-Directed Control of c-Myc Functions: Understanding the Balance from Proliferation to Growth Arrest
by Agata Kubickova, Juan Bautista De Sanctis and Marian Hajduch
Int. J. Mol. Sci. 2023, 24(24), 17524; https://doi.org/10.3390/ijms242417524 - 15 Dec 2023
Viewed by 874
Abstract
The transcription factor c-Myc, a key regulator of cellular processes, has long been associated with roles in cell proliferation and apoptosis. This review analyses the multiple functions of c-Myc by examining the different c-Myc isoforms in detail. The impact of different c-Myc isoforms, [...] Read more.
The transcription factor c-Myc, a key regulator of cellular processes, has long been associated with roles in cell proliferation and apoptosis. This review analyses the multiple functions of c-Myc by examining the different c-Myc isoforms in detail. The impact of different c-Myc isoforms, in particular p64 and p67, on fundamental biological processes remains controversial. It is necessary to investigate the different isoforms in the context of proto-oncogenesis. The current knowledge base suggests that neoplastic lesions may possess the means for self-destruction via increased c-Myc activity. This review presents the most relevant information on the c-Myc locus and focuses on a number of isoforms, including p64 and p67. This compilation provides a basis for the development of therapeutic approaches that target the potent growth arresting and pro-apoptotic functions of c-Myc. This information can then be used to develop targeted interventions against specific isoforms with the aim of shifting the oncogenic effects of c-Myc from pro-proliferative to pro-apoptotic. The research summarised in this review can deepen our understanding of how c-Myc activity contributes to different cellular responses, which will be crucial in developing effective therapeutic strategies; for example, isoform-specific approaches may allow for precise modulation of c-Myc function. Full article
(This article belongs to the Special Issue MYC and p53 Gene Families)
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