Novel Drugs that Target ErbB2

Abstract

Betulinic acid (BA) is a triterpenoid anticancer agent, and treatment of epidermal growth factor 2 (EGFR2, HER2/ErbB2)- overexpressing BT474 and MDA-MB-453 cells with 1-10 micrometers BA inhibited cell growth and induced apoptosis. BA also induced proteasome-independent downregulation of specificity protein (Sp) transcription factors Sp1, Sp3, Sp4 and survivin, a Sp-regulated gene, and decreased expression of ErbB2, ErbB2-regulated kinases and YY1, a transcription factor that regulates ErbB2 expression. Knockdown of Sp1, Sp3, Sp4 and their combination by RNA interference was accompanied by decreased expression of ErbB2, YY1 and luciferase activity in cells transfected with a construct containing the GC-rich YY1 promoter linked to a luciferase reporter gene. BA-dependent repression of Sp1, Sp3, Sp4 and Sp regulated genes was due, in part, to induction of the Sp repressor ZBTB10 and downregulation of microRNA-27a (miR-27a) which constitutively inhibits ZBTB10 expression. The effects of BA on the miR-27a:zBTB10-Sp transcription factor axis were inhibited in cells cotreated with the cannabinoid 1 (CB1) and CB2 receptor antagonists AM251 and AM630, respectively. However, in vitro binding studies with <=10 micrometers BA and a radiolabled cannabinoid did not indicate competitive binding of BA to the CB1 and CB2 receptors, suggesting a possible role for other CB-like G protein-coupled receptors.

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Document Details

Document Type
Technical Report
Publication Date
May 01, 2011
Accession Number
ADA547599

Entities

People

  • Stephen Safe

Organizations

  • Texas A&M University

Tags

DTIC Thesaurus Topics

  • Abstracts
  • Acids
  • Antineoplastic Agents
  • Apoptosis
  • Breast Cancer
  • Cell Line
  • Department Of Defense
  • Drug Abuse
  • Fatty Acids
  • Inhibition
  • Inhibitors
  • Instructions
  • Neoplasms
  • Plant Oils
  • Prostate Cancer
  • Proteins
  • Transcription Factors

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.
  • Cellular and Molecular Pathways of Apoptosis.
  • Materials Science and Engineering.