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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
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Updated: Mar 13, 2026

In vitro Transcription and Capping of Gaussia Luciferase mRNA Followed by HeLa Cell Transfection
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c-Myc deregulation induces mRNA capping enzyme dependency.

Olivia Lombardi1, Dhaval Varshney1, Nicola M Phillips1,2

  • 1Centre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.

Oncotarget
|October 21, 2016
PubMed
Summary

Myc oncogene drives cancer by upregulating mRNA capping enzyme (CE). Inhibiting CE selectively targets cancer cells with deregulated Myc, offering a new therapeutic strategy.

Keywords:
c-Myccell proliferationmRNA captranscriptiontranslation

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • c-Myc is a key driver in numerous human cancers.
  • Directly targeting c-Myc has yielded limited therapeutic success.
  • Investigating upstream regulators and downstream effectors of c-Myc is a promising alternative strategy.

Purpose of the Study:

  • To elucidate the mechanism by which c-Myc enhances mRNA capping.
  • To investigate the role of mRNA capping enzyme (CE) in c-Myc-driven cancers.
  • To evaluate CE inhibition as a potential therapeutic strategy for cancers with deregulated c-Myc.

Main Methods:

  • Investigated the interaction between c-Myc and mRNA capping enzyme (CE/RNGTT).
  • Assessed the impact of c-Myc on CE recruitment to RNA polymerase II and target genes.
  • Evaluated the dependency of c-Myc-induced gene expression, proliferation, and transformation on CE activity.

Main Results:

  • c-Myc enhances the recruitment of catalytically active CE to RNA polymerase II and target genes.
  • c-Myc-driven gene expression, cell proliferation, and transformation are critically dependent on CE when c-Myc is deregulated.
  • Normal c-Myc expression control renders cells insensitive to CE repression, while c-Myc expression itself is CE-dependent.

Conclusions:

  • c-Myc upregulates mRNA capping by increasing CE recruitment to target genes.
  • Inhibiting CE selectively targets cancer cells with deregulated c-Myc.
  • CE inhibition represents an attractive therapeutic approach for specific cancer types.