Physiological Stree-Induced Drug Resistance and Its Reversal

Abstract

Physiologic induced drug resistance to topoisomerase II inhibitors was studied in EMT6 mouse mammary tumor cell lines created under the award. EMT6 cells transfected with ponasterone A inducible plasmids containing either the p65 subunit of NFkB or the p50 subunit of NEkE or the non-phosphorylatable mutant of IkE were assessed for NEkE activation and drug resistance in the presence or absence of stress. Expression of the p65 or p50 subunits resulted in drug resistance to etoposide and doxorubicin. Expression of the IkE mutant which prevents the activation of NEkE blocked the development of stress induced drug resistance. These data demonstrate that NEkE is necessary and sufficient for the development of stress induced resistance.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2001
Accession Number
ADA398214

Entities

People

  • Katherine A. Kennedy

Organizations

  • George Washington University

Tags

DTIC Thesaurus Topics

  • Albumins
  • Antineoplastic Agents
  • Blood
  • Breast Cancer
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Chemotherapy
  • Drug Resistance
  • Electronic Mail
  • Health Services
  • Indicator Dyes
  • Neoplasms
  • Pharmacology
  • Proteins
  • Stress (Physiology)

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.
  • Oncology (Cancer Research).
  • Trauma Surgery or Emergency Medicine.