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In vivo Application of the REMOTE-control System for the Manipulation of Endogenous Gene Expression
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In vivo Application of the REMOTE-control System for the Manipulation of Endogenous Gene Expression

Published on: March 29, 2019

Vinorelbine induces beta3-tubulin gene expression through an AP-1 Site

Jennifer Saussede-Aim1, Eva-Laure Matera, Stephanie Herveau

  • 1Laboratoire de Cytologie Analytique, Faculté de Medecine Rockefeller, 8 Avenue Rockefeller, 69008 Lyon, France. jennifer.saussede-aim@laposte.net

Anticancer Research
|August 8, 2009
PubMed

Insights

Beta3-tubulin gene expression is inducible by antimicrotubule agents. A specific vinorelbine-responsive element containing an activator protein 1 (AP-1) site was identified in the beta3-tubulin gene promoter.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Pharmacology

Background:

  • Beta3-tubulin expression correlates with clinical outcomes in patients treated with microtubule-targeted agents.
  • The regulatory mechanisms governing beta3-tubulin expression are not well understood.
  • Gene promoter cloning provided new insights into beta3-tubulin regulation.

Purpose of the Study:

  • To investigate the regulation of beta3-tubulin gene expression.
  • To identify specific DNA elements responsible for the induction of beta3-tubulin.
  • To understand the role of the beta3-tubulin gene promoter in response to antimicrotubule agents.

Main Methods:

  • Beta3-tubulin gene expression was induced using antimicrotubule agents like vinorelbine and paclitaxel.
  • Successive deletions and site-directed mutagenesis were employed to analyze the beta3-tubulin gene promoter.
  • Identification of a vinorelbine-responsive element (VRE) within the promoter region.

Main Results:

  • Beta3-tubulin gene expression was induced by vinorelbine and paclitaxel.
  • A vinorelbine-responsive element containing an activator protein 1 (AP-1) site was localized in the beta3-tubulin promoter.
  • This specific AP-1 site was activated exclusively by vinorelbine exposure among the tested agents.

Conclusions:

  • The beta3-tubulin gene promoter exhibits inducible characteristics.
  • Vinorelbine specifically activates a distinct AP-1 site within the beta3-tubulin promoter, contributing to its induction.
  • These findings enhance the understanding of beta3-tubulin gene regulation in response to therapeutic agents.

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