Mechanism of Growth Factor Attenuation of Cell Death in Chemotheraphy Treated Breast Cancer Cells

Abstract

Upregulation of IGF-I (Insulin-like Growth Factor) receptor dependent pathways like phosphatidylinositol 3-kinase (PI 3-kinase) may diminish chemosensitivity of breast cancer cells via c- Jun N-terminal Kinase (JNK) response. In this project we have determined that IGF-I activates the survival pathway involving PI 3-kinase and Akt. Using stable transfection approaches we have confirmed the survival effect of activated Aict in MCF-7 cells. Surprisingly, we have also observed that IGF-I induces JNK in breast cancer cells. IGF-I and chemotherapy co-treatment results in additive effect on JNK activity, in contrast to our predicted results that IGF-I would antagonize chemotherapy induced JNK activity. PI 3-kinase mediates IGF-I induction of JNK in MCF-7 cells but not in T47D cells. We plan to further confirm the importance of JNK in IGF-I mediated survival effects in breast cancer cells.

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Document Details

Document Type
Technical Report
Publication Date
Aug 01, 2001
Accession Number
ADA400582

Entities

People

  • Carla Vandenberg

Organizations

  • University of Colorado Health

Tags

DTIC Thesaurus Topics

  • Apoptosis
  • Attenuation
  • Biomedical Research
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemotherapy
  • Contrast
  • Culture Techniques
  • Diseases And Disorders
  • Growth Factors
  • Neoplasms
  • Neuropathy
  • Survival
  • Tumor Cell Line

Fields of Study

  • Medicine

Readers

  • Breast cancer cell signaling and growth regulation.
  • Oncology (Cancer Research).