The Myc/Max/Mad Transcription Factor Network

Eisenman, Robert N.

doi:10.1007/3-540-32952-8

Current Topics in Microbiology and Immunology

2006

DOI: 10.1007/3-540-32952-8

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The Myc/Max/Mad Transcription Factor Network

Robert N. Eisenman¹

Abstract: Cover Illustration: The cover figure depicts a Myc-Max protein heterodimer interacting with its CACGTG binding site in DNA, superimposed over an image of DAPI-stained cell nuclei. The large cell nuclei are located within a Drosophila larval salivary gland ectopically expressing Drosophila Myc (dMyc) while the small nuclei are from fat body cells lacking ectopic dMyc (from Pierce SB,

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Cited by 6 publications

References 352 publications

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Myc, Mondo, and Metabolism

Sloan

Ayer

2010

Genes & Cancer

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The Myc family of proto-oncogenes plays a central role in tumorigenesis, yet identifying the specific transcriptional targets required for its oncogenic function remains a challenge. Given Myc’s broad role in transcriptional regulation, it seems unlikely that there exists one or even a small set of Myc effectors strictly required for transformation. Over the last decade or so, it has become clear that Myc can drive several metabolic pathways associated with cell growth. There is compelling evidence that Myc regulates these pathways directly and that their regulation is not an epiphenomenon. As such, for understanding Myc’s pleiotropic role in cell growth, cell division, and cell death, it may be fruitful to focus more broadly on Myc-regulated pathways than on specific targets. Myc was first shown to regulate glycolysis, but it is now clear that Myc regulates many biosynthetic pathways required for cell growth and division. A related family of transcriptional regulators, the Mondo family, has recently been discovered that may interact with members of the Myc family to control cell growth. The Mondo family is a key sensor of intracellular bioenergetic charge, and one function appears to be in controlling the availability and utilization of intracellular glucose. Here we focus on the metabolic pathways regulated by Myc and Mondo and speculate on the largely unexplored question of their cooperation in controlling cancer cell metabolism.

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Myc, Mondo, and Metabolism

Sloan

Ayer

2010

Genes & Cancer

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Role of MXD3 in Proliferation of DAOY Human Medulloblastoma Cells

et al. 2012

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A subset of medulloblastomas, the most common brain tumor in children, is hypothesized to originate from granule neuron precursors (GNPs) in which the sonic hedgehog (SHH) pathway is over-activated. MXD3, a basic helix-look-helix zipper transcription factor of the MAD family, has been reported to be upregulated during postnatal cerebellar development and to promote GNP proliferation and MYCN expression. Mxd3 is upregulated in mouse models of medulloblastoma as well as in human medulloblastomas. Therefore, we hypothesize that MXD3 plays a role in the cellular events that lead to medulloblastoma biogenesis. In agreement with its proliferative role in GNPs, MXD3 knock-down in DAOY cells resulted in decreased proliferation. Sustained overexpression of MXD3 resulted in decreased cell numbers due to increased apoptosis and cell cycle arrest. Structure-function analysis revealed that the Sin3 interacting domain, the basic domain, and binding to E-boxes are essential for this activity. Microarray-based expression analysis indicated up-regulation of 84 genes and down-regulation of 47 genes. Potential direct MXD3 target genes were identified by ChIP-chip. Our results suggest that MXD3 is necessary for DAOY medulloblastoma cell proliferation. However, increased level and/or duration of MXD3 expression ultimately reduces cell numbers via increased cell death and cell cycle arrest.

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C-Myc Signaling Pathway in Treatment and Prevention of Brain Tumors

Ashrafizadeh

Zarabi

Hushmandi

et al. 2021

CCDT

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: Brain tumors are responsible for high morbidity and mortality worldwide. Several factors such as the presence of blood-brain barrier (BBB), sensitive location in the brain, and unique biological features challenge the treatment of brain tumors. The conventional drugs are no longer effective in the treatment of brain tumors, and scientists are trying to find novel therapeutics for brain tumors. In this way, identification of molecular pathways can facilitate finding an effective treatment. c-Myc is an oncogene signaling pathway capable of regulation of biological processes such as apoptotic cell death, proliferation, survival, differentiation, and so on. These pleiotropic effects of c-Myc have resulted in much fascination with its role in different cancers, particularly brain tumors. In the present review, we aim to demonstrate the upstream and down-stream mediators of c-Myc in brain tumors such as glioma, glioblastoma, astrocytoma, and medulloblastoma. The capacity of c-Myc as a prognostic factor in brain tumors will be investigated. Our goal is to define an axis in which the cMyc signaling pathway plays a crucial role and to provide direction for therapeutic targeting in these signaling networks in brain tumors.

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The Myc/Max/Mad Transcription Factor Network

Cited by 6 publications

References 352 publications

Myc, Mondo, and Metabolism

Myc, Mondo, and Metabolism

Role of MXD3 in Proliferation of DAOY Human Medulloblastoma Cells

C-Myc Signaling Pathway in Treatment and Prevention of Brain Tumors

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