Molecular Biology Associated with c-Myc

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

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 3935

Special Issue Editor


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Guest Editor
College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea
Interests: c-Myc; c-Myc target gene; regulation of c-Myc; ribosomal proteins; natural compound; apoptosis; metastasis; EMT; cancer stem cell
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Special Issue Information

Dear Colleagues,

Among oncogenic molecules, Myc is elevated or dysregulated in about 70% of human cancers. MYC oncogene family comprising of C-Myc, N-Myc, L-Myc and S-Myc. Among four types of Myc genes, c-Myc is the most oncogenic gene in several cancer cells.

c-Myc oncoprotein is a regulatory factor of cancer cell growth and proliferation. Activation of c-Myc has an important role in cancer development by transcriptionally regulating a number of genes that are involved in cell division, cell survival and ribosome biogenesis. The main focus of this Special Issue will be on the broad spectrum of functions of c-Myc in cancer cells.

We invite all scientists working on c-Myc to participate in this special issue. Original research articles or reviews on all aspects of the molecular and cellular mechanisms modulated by c-Myc in cancer cells are welcome.

We look forward to your contributions.

Prof. Dr. Ji Hoon Jung
Guest Editor

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Keywords

  • c-Myc
  • MYC
  • cancer
  • apoptosis
  • novel gene
  • natural compound
  • cancer therapy
  • c-Myc target gene
  • cancer stem cell
  • ribosome biogenesis

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Published Papers (1 paper)

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Research

18 pages, 2930 KiB  
Article
A Drug Repurposing Screen Identifies Fludarabine Phosphate as a Potential Therapeutic Agent for N-MYC Overexpressing Neuroendocrine Prostate Cancers
by Hussain Elhasasna, Raymond Khan, Kalpana K. Bhanumathy, Frederick S. Vizeacoumar, Prachi Walke, Maricris Bautista, Dinesh K. Dahiya, Vincent Maranda, Hardikkumar Patel, Amrutha Balagopal, Nezeka Alli, Anand Krishnan, Andrew Freywald and Franco J. Vizeacoumar
Cells 2022, 11(14), 2246; https://doi.org/10.3390/cells11142246 - 20 Jul 2022
Cited by 7 | Viewed by 3110
Abstract
Neuroendocrine prostate cancer (NEPC) represents a highly aggressive form of prostate tumors. NEPC results from trans-differentiated castration-resistant prostate cancer (CRPC) with increasing evidence indicating that the incidence of NEPC often results from the adaptive response to androgen deprivation therapy. Recent studies have shown [...] Read more.
Neuroendocrine prostate cancer (NEPC) represents a highly aggressive form of prostate tumors. NEPC results from trans-differentiated castration-resistant prostate cancer (CRPC) with increasing evidence indicating that the incidence of NEPC often results from the adaptive response to androgen deprivation therapy. Recent studies have shown that a subset of NEPC exhibits overexpression of the MYCN oncogene along with the loss of tumor suppressing TP53 and RB1 activities. N-MYC is structurally disordered with no binding pockets available on its surface and so far, no clinically approved drug is available. We adopted a drug-repurposing strategy, screened ~1800 drug molecules, and identified fludarabine phosphate to preferentially inhibit the proliferation of N-MYC overexpressing NEPC cells by inducing reactive oxygen species (ROS). We also show that fludarabine phosphate affects N-MYC protein levels and N-MYC transcriptional targets in NEPC cells. Moreover, enhanced ROS production destabilizes N-MYC protein by inhibiting AKT signaling and is responsible for the reduced survival of NEPC cells and tumors. Our results indicate that increasing ROS production by the administration of fludarabine phosphate may represent an effective treatment option for patients with N-MYC overexpressing NEPC tumors. Full article
(This article belongs to the Special Issue Molecular Biology Associated with c-Myc)
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